Chemopreventive phytochemicals & Cancer (flavonoids, herbs, resveratrol, curcumin, EGCG, berberine, piperine , sulforaphane, capsaicin, folate, quercetin, fisetin , genistein, alpha & beta carotene, PUFAs, vit D3, etc. – many studies show anti-cancer properties of these)
Phytochemicals and Cancer
: (26)
It is estimated that an average of 35% of human cancers (certain
types up to 70%) can be attributed to diet (
1
), and
epidemiological research has shown a link in the geographical distribution of
cancer incidence to specific diet consumption. According to the World Health
Organization report 2002, there are at least 2.7 million deaths globally per
year, which are primarily attributable to low fruit and vegetable intake (
2
). This
is not surprising, as the National Cancer Institute identified about 35
plant-based foods that possess anti-cancer benefits, including garlic,
soybeans, ginger, onion, turmeric, tomatoes, and cruciferous vegetables
(broccoli, cabbage, cauliflower, and Brussels sprouts). Furthermore, the
chemopreventive
efficacy of these diet constituents has
been demonstrated
in vitro
and
in vivo
. The
substantial anticarcinogenic and antimutagenic properties of these tested
dietary agents can be attributed to the non-nutritive components of these
foods, termed
phytochemicals
. There could be more than 100
different phytochemicals in just a single serving of vegetables (
2
), and
they can be extracted for therapeutic purposes. Since phytochemicals have not
been shown to have any known toxicities, they can be considered as an
alternative to the conventional chemotherapy that may be harmful. A number of
phytochemicals have been found to have notable efficacy in preclinical models
of carcinogenesis, such as those of
colorectum, breast, lung, and
hematological origin.
These include epigallocatechin gallate
(EGCG)
from
tea, the flavonoids
quercetin
and
genistein
from
onions and soya,
curcumin
in curry spice
and
resveratrol
from red grapes (
3
).
Chemopreventive
phytochemicals
can block
the initiation or reverse the promotion of carcinogenesis and impede the progression
of precancerous cells into malignant ones.
[Natural Chemoprevention of Cancer:
AMP-activated
protein kinase (AMPK) is an energy sensor that plays a key role in the
regulation of protein and lipid metabolism in response to changes in fuel
availability
(
9
-
11
)
.
An extensive body of evidence has demonstrated
that AMPK inhibits essentially all anabolic pathways that promote cell growth,
such as synthesis of fatty acid, phospholipid, protein, and ribosomal RNA
synthesis
( HYPERLINK
"https://www.frontiersin.org/articles/10.3389/fonc.2013.00175/full"
\l "B12" 12
,
HYPERLINK
"https://www.frontiersin.org/articles/10.3389/fonc.2013.00175/full"
\l "B13" 13). Thus, it is not surprising that AMPK antagonizes cancer
cell growth.
When activated, AMPK promotes energy-producing catabolic pathways
while inhibiting anabolic pathways, such as cell growth and proliferation
thereby antagonizing carcinogenesis. Other anti-cancer effects of AMPK may
include promoting autophagy and DNA repair upon UVB damage.
Since
the
AMPK cascade has emerged as an important pathway implicated in
cancer control
, many discoveries have been made in the past decade
revealing robust anti-cancer effects of AMPK
in vitro
and
in
vivo
, including animal cancer models of breast, lung, colorectum, skin, and
hematological malignancies.
Among the latest developments is the activation of AMPK by
naturally occurring dietary constituents and plant
products
termed
phytochemicals
.
Owing to their efficacy and safety, phytochemicals are considered as an
alternative
to the conventional harmful chemotherapy
.
A number of phytochemicals have been found to have notable
efficacy in preclinical models of carcinogenesis, such as those of colorectum,
breast, lung, and hematological origin. These include epigallocatechin gallate
(EGCG) from tea, the flavonoids quercetin and genistein from onions and soya,
curcumin in curry spice and resveratrol from red grapes.
Chemopreventive
phytochemicals can block the initiation or reverse the promotion of
carcinogenesis and impede the progression of precancerous cells into malignant
ones. Metformin, the most widely prescribed Type-2 diabetes drug for more than
30 years, has been shown to activate AMPK
(
22
,
23
).
Consistent
with this, diabetic patients treated with metformin had a lower incidence of
cancer compared to those on other medications. A recent study showed that
breast cancer patients on metformin for diabetes responded significantly better
to chemotherapy than other diabetic patients not on metformin and non-diabetic
patients
(
26
).
Human cell line studies and animal studies using these phytochemicals have
shown promising results activating AMPK for several types of cancer
(
27
)
.
Metformin
treatment led to increased apoptosis in human
lung cancer
cell
lines and significantly inhibited cell proliferation in a dose- and
time-dependent manner(
51
). Metformin
had similar results in animal studies for lung
cancer.AMPK
has been shown
to
inhibit
cancer cell growth in various hematological cancers. Metformin use
resulted in a strong anti-leukemic activity against primary Acute Myeloid
Leukemia cells while sparing normal hematopoiesis
ex vivo
and
significantly reducing the growth of AML cells in a mouse study(
51
). Zhang
and Bowden reported that UVB irradiation, a strong carcinogen for
non-melanoma
skin cancer
, reduced activation of AMPK, leading to
increased Cox-2 mRNA stability, which may contribute to cancer development
(
63
).
In
UVB-damaged tumor-bearing mice, both topical and systemic metformin prevented
the formation of new tumors and suppressed growth of established tumors,
demonstrating that AMPK acts as a tumor suppressor in the skin by promoting DNA
repair and controlling cell proliferation (
43
).
Curcumin
has
been shown to suppress tumor progression in various animal models of cancer
(
64
-
67
). Recently,
AMPK was found to be a new molecular target of curcumin. Pan et al(
67
).
showed that activation of AMPK by curcumin has shown to be responsible for the
cytotoxic effects of curcumin in
ovarian cancer cells
. Curcumin is
a potent stimulator of AMPK leading to chemoprevention(
66
). Anti-cancer, anti-inflammatory,
blood sugar-lowering, and other beneficial cardiovascular effects of
resveratrol
have
been reported in animal models and human clinical trials
(
68
-
71
). AMPK is now a
recognized target of resveratrol that mediates its anti-cancer effects(
72
-
74
).
Flavonoids
can be found in many different sources, including soy, berries, tea, wine,
beer, chocolate, many vegetables, and most fruits. While there are several 1000
types, they can be categorized as
flavones
(quercetin,
fisetin
, luteolin),
isoflavonoids
(genistein,
deguelin), and
neoflavonoids
(
81
).
The
chemopreventive
effects of a soy
isoflavonoid
genistein
can
be attributed to its ability to activate AMPK(
82
).
Anthocyanin
belonging to the family of flavones that occurs in all tissues of higher
plants, including leaves, stems, roots, flowers, and fruits is shown to be a
powerful activator of AMPK(
84
)According
to studies,
Fisetin
, a
flavonoid,
activates AMPK to induce apoptosis in
multiple
myeloma
cells(
85
),
inhibits PI3K/AKT and mTOR and activates AMPK in non-small cell
lung
cancer
(
86
),
and
induces autophagy-mediated cell death by activating AMPK and suppressing mTOR
in
prostate cancer
cells
(
87
)
.
Quercetin
induces
apoptosis via AMPK activation and p53 in HT-29
colon cancer cells(
88
)
�Similar
for other flavonoids. Epigallocatechin-3-gallate,
EGCG,
a
green tea-derived polyphenol, has been shown to
suppress cancer cell
proliferation
and interfere with the several signaling pathways and
induce apoptosis. EGCG treatment of HT-29
colon
cancer
cells
resulted in a strong activation of AMPK and an inhibition of COX-2 expression (
95
). Moreover,
analogs of EGCG have been synthesized and found to be more potent AMPK
activators than metformin and EGCG.
Activation
of AMPK by these EGCG analogs resulted in the inhibition of cell proliferation,
up-regulation of the cyclin-dependent kinase inhibitor p21, and suppression of
stem cell population in human
breast cancer cells
. Furthermore,
EGCG was shown to enhance the anti-tumor activity of 5-fluorouracil (5-FU), one
of the most commonly used chemotherapeutic drugs, suggesting that EGCG may be
used as an adjunct therapy for the treatment of advanced-stage liver cancer (
98
).
Berberine
,
a traditional plant alkaloid used in Ayurvedic and Chinese medicine for its
antimicrobial and antiprotozoal properties, strongly
increased AMPK
phosphorylation
via ROS production, leading to inhibition of tumor
cell adhesion, tumor invasion, and the expression of epithelial to mesenchymal
transition (EMT)-related genes
.
Furthermore,
berberine
inhibited the metastatic potential
of melanoma cells through a
decrease in ERK activity and protein levels of cyclooxygenase-2 (COX-2) by a
berberine-induced AMPK activation (
99
). In another
study,
berberine
was shown to inhibit migration of
colon
cancer cells
in an AMPK-dependent manner (
100
). Furthermore,
24-
hydroxyursolic
acid from persimmon,
capsaicin
, and p-HPEA-EDA, a phenolic compound
of virgin olive oil, activate AMPK and inhibit cell survival in HT-29
colon
cancer
cells (
100
,
103
).
In
summary, the use of phytochemicals derived from dietary agents holds promise in
the prevention and treatment of cancer, and AMPK is one of the major pathways
activated by many phytochemicals. Not only do
phytochemicals activate
AMPK to increase cancer cell apoptosis and inhibit cell proliferation,
but
they have also been shown to be effective in reducing the toxicity associated
with standard chemotherapy by increasing the sensitivity of cancer cells to
drugs. [ Taken from (25), references are per that study, click on number
to see reference]
https://www.nutritionalconference.com/speaker-keynote-pdfs/2015/gary-stoner-medical-college-of-wisconsin-usa.pdf
; &
(c )
WebMD-� cancer
prevention, .
https://www.webmd.com/cancer/features/seven-easy-to-find-foods-that-may-help-fight-cancer#1
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
In Vivo.
2019
Jul-Aug;33(4):983-997.
doi
: 10.21873/invivo.11568.
1
The London
Breast Institute, Princess Grace Hospital, London, U.K.
kefahmokbel@hotmail.com.
2
The
London Breast Institute, Princess Grace Hospital, London, U.K.
Numerous dietary components and vitamins have been found to
inhibit the molecular events and
signalling
pathways
associated with various stages of breast
cancer
development.
To identify the vitamins and dietary micronutrients that exert protective
effects against breast
cancer
and
define their mechanism of action, we performed a literature review of in vitro,
animal and epidemiological studies and selected the in vitro and animal studies
with robust molecular evidence and the epidemiological studies reporting
statistically significant inverse associations for a breast
cancer
-specific
protective effect. There is sufficient evidence from in vitro, animal and
epidemiological human studies that certain vitamins, such as vitamin
D3,
folate, vitamin B6, and beta carotene as well as dietary micronutrients, such
as curcumin,
piperine
, sulforaphane,
indole-3-carbinol, quercetin, epigallocatechin gallate (
EGCG
)
and omega-3 polyunsaturated fatty acids (PUFAs)
, display an
antitumoral
activity against breast
cancer
and
have the potential to offer a natural strategy for breast
cancer
chemoprevention and reduce the risk of
breast
cancer
recurrence. Therefore, a supplement
that contains these micronutrients, using the safest form and dosage should be
investigated in future
breast
cancer
chemoprevention
studies and as part of standard breast
cancer
therapy.
Resveratrol.
https://www.ncbi.nlm.nih.gov/pubmed/?term=resveratrol+cancer
;
Cancer
Cell
Int.
2019 Jul
15;19:180
.
doi
:
10.1186/s12935-019-0906-y.
eCollection
2019.
Honari
M
1
,
Shafabakhsh
R
1
,
Reiter RJ
2
,
Mirzaei H
1
,
Asemi
Z
1
.
Int J Pharm.
2019
Aug 5:118599.
doi
: 10.1016/j.ijpharm.2019.118599. [
Epub
ahead of print]
Al-Attar T
1
,
Madihally
SV
2
.
EGCG
Cancer
:
https://www.ncbi.nlm.nih.gov/pubmed/?term=egcg+cancer
;
(dozens)
Colon
cancer:
Nanomedicine.
2019 Jul
30:102068.
doi
: 10.1016/j.nano.2019.102068. [
Epub
ahead of print]
Wang R
1
,
Huang J
2
,
Chen J
3
,
Yang M
4
,
Wang H
5
,
Qiao
H
6
,
Chen Z
7
,
Hu L
8
,
Di L
9
,
Li J
10
.
Abstract
Colon adenocarcinoma is the third most common cause
of cancer-related deaths worldwide owing to its aggressive nature. Here,
we developed a novel oral drug delivery system (DDS) that comprised active
targeted nanoparticles made from gelatin and chitosan (non-toxic polymers). The
nanoparticles were fabricated using a complex coacervation method, which was
accompanied by conjugation of wheat germ agglutinin (WGA) onto their surface by
glutaraldehyde cross-linking. Specifically, we integrated 5-fluorouracil
(5-FU), the first-line treatment agent against colon cancer, and
(-)-epigallocatechin-3-gallate (EGCG), which inhibits tumor growth via
anti-angiogenesis and apoptosis-inducing effects, into the nanoparticles, named
WGA-EF-NP. The 5-FU and EGCG co-loaded nanoparticles showed sustained
drug release, enhanced cellular uptake, and longer circulation time. WGA-EF-NP
exhibited superior anti-tumor activity and pro-apoptotic efficacy compared to
the drugs and nanoparticles without WGA decoration owing to better
bioavailability and longer circulation time in vivo. Thus,
WGA-EF-NP shows
promise as a DDS for enhanced efficacy against colon cancer.
Cells.
2019 Jul
19;8(7).
pii
: E745.
doi
:
10.3390/cells8070745.
Zhang L
1
,
He Y
1
,
Wu X
1
,
Zhao G
1
,
Zhang K
1
,
Yang CS
2
,
Reiter RJ
3
,
Zhang J
4
.
Abstract
We have demonstrated previously that melatonin
attenuates hepatotoxicity triggered by high doses of
(-)-epigallocatechin-3-gallate (EGCG) in mice. The current work investigated
the influence of melatonin on the
oncostatic
activity
of EGCG in two cancer cell lines, wherein melatonin induced
an opposite response of p21. In human tongue cancer TCA8113 cells,
melatonin-induced p21 and EGCG-mediated formation of
quinoproteins
were positively associated with the
oncostatic
effects of melatonin and EGCG. Melatonin-stimulated an increase in p21
which was correlated with a pronounced nuclear translocation of thioredoxin 1
and thioredoxin reductase 1, both of which are known to induce p21 via
promoting p53 trans-activation. Melatonin did not influence
the EGCG-mediated increase of
quinoprotein
formation nor did EGCG impair melatonin-induced p21 up-regulation.
Co-treatment with both agents enhanced the cell-killing effect as well as the
inhibitory activities against cell migration and colony formation. It is known
that p21 also plays a powerful anti-apoptotic role in
some cancer cells and confers these cells with a survival advantage,
making it a target for therapeutic suppression. In human hepatocellular
carcinoma HepG2 cells, melatonin suppressed p21 along with the induction of
pro-survival proteins, PI3K and COX-2. However,
EGCGprevented
against melatonin-induced PI3K and COX-2, and melatonin probably sensitized
HepG2 cells to
EGCGcytotoxicity
via
down-regulating p21, Moreover, COX-2 and HO-1 were significantly reduced only
by the co-treatment, and melatonin aided EGCG to achieve an increased
inhibition on Bcl2 and
NFκB
. These events occurring
in the co-treatment collectively resulted in an enhanced cytotoxicity. In
addition, the co-treatment also enhanced the inhibitory activities against cell
migration and colony formation. Overall, the results gathered from these
two cancer cell lines with a divergent p21 response to melatonin show
that the various
oncostatic
activities of
melatonin and EGCG together are more robust than each agent alone,
suggesting
that they may be useful partners in fighting cancer.
Ther
Deliv
.
2019 Jul;10(7):409-417.
doi
: 10.4155/tde-2019-0015.
Epub
2019 Jul 19.
Rosita N
1
,
Meitasari
VA
1
,
Rianti
MC
1
,
Hariyadi
DM
1
,
Miatmoko
A
1
.
1
Department of Pharmaceutics,
Faculty of Pharmacy, Universitas
Airlangga
,
Kampus
C
Mulyorejo
, Surabaya
60115, Indonesia.
Aim:
(-)-Epigallocatechin
gallate (
EGCG
) has been reported as inducing
apoptosis in cervical
cancer
. However,
EGCG
demonstrates
low skin permeability. In order to develop topical delivery of
EGCG
, the
partition coefficient, log P, was modified using a reverse micelle method.
Results & methodology:
During this study, Tween 80 and Span
80 were added to
EGCG
at
hydrophilic-lipophilic balance (HLB) values of 4.3, 6 and 8. The results showed
that lowering the HLB value increases the log P value of
EGCG
and results in higher IC
50
values in Henrietta Lacks (HeLa)
cancer
cells
than that of
EGCG
.
Surfactant-modified
EGCG
-HLB 6 produced faster and deeper skin penetration
than
EGCG
.
Conclusion:
Modification of log P value using a
combination of Tween 80 and Span 80 improved cytotoxicity and topical delivery
of
EGCG
.
Bioengineered.
2019 Dec;10(1):282-291.
doi
: 10.1080/21655979.2019.1632669.
Li T
1
,
Zhao N
2
,
Lu J
2
,
Zhu Q
2
,
Liu X
3
,
Hao F
4
,
Jiao X
5
.
Transforming growth factor (TGF)-β1 plays a crucial role in the epithelial-to-mesenchymal
transition (EMT) in many
cancer
types
and in thyroid cancers. Epigallocatechin-3-gallate (
EGCG
),
the most important ingredient in the green tea, has been reported to possess
antioxidant and anticancer activities. However, the cellular and molecular
mechanisms explaining its action have not been completely understood. In this
study, we found that
EGCG
significantly
suppresses
EMT, invasion and migration in a
naplastic thyroid carcinoma
(ATC) 8505C
cells
in vitro
by regulating the TGF-β/
Smad
signaling pathways.
EGCG
significantly
inhibited TGF-β1-induced expression of EMT markers (E-cadherin reduction and
vimentin induction) in 8505C cells
in
vitro
. Treatment with
EGCG
completely
blocked the phosphorylation of Smad2/3, translocation of Smad4. Taken together,
these results suggest that
EGCG
suppresses EMT and invasion and migration
by blocking TGFβ/
Smad
signaling pathways.
ACS Nano.
2019 Jul 23;13(7):7591-7602.
doi
: 10.1021/acsnano.9b00467.
Epub
2019 Jul 8.
Yongvongsoontorn
N
1
,
Chung JE
1
,
Gao SJ
1
,
Bae KH
1
,
Yamashita A
1
,
Tan MH
1
,
Ying JY
1
,
Kurisawa
M
1
.
1
Institute of Bioengineering and
Nanotechnology ,
31
Biopolis
Way,
The Nanos, #07-01 , Singapore 138669.
Although a few nanomedicines have been approved for clinical use
in
cancer
treatment, that recognizes improved
patient safety through targeted delivery, their improved efficacy over
conventional drugs has remained marginal. One of the typical drawbacks of
nanocarriers for
cancer
therapy
is a low drug-loading capacity that leads to insufficient efficacy and requires
an increase in dosage and/or frequency of administration, which in turn
increases carrier toxicity. In contrast, elevating drug-loading would cause the
risk of nanocarrier instability, resulting in low efficacy and off-target
toxicity. This intractable drug-to-carrier ratio has imposed constraints on the
design and development of nanocarriers. However, if the nanocarrier has
intrinsic therapeutic effects, the efficacy would be synergistically augmented
with less concern for the drug-to-carrier ratio. Sunitinib-loaded micellar
nanocomplex (SU-MNC) was formed using
poly(
ethylene
glycol)-conjugated epigallocatechin-3-
O
-gallate (PEG-
EGCG
) as such a carrier. SU-MNC specifically inhibited
the vascular endothelial growth factor-induced proliferation of endothelial
cells, exhibiting minimal cytotoxicity to normal renal cells.
SU-MNC showed
enhanced anticancer effects and less toxicity than SU administered
orally/intravenously on human renal cell carcinoma-xenografted mice,
demonstrating more efficient effects on anti-angiogenesis, apoptosis induction,
and proliferation inhibition against tumors. In comparison, a conventional
nanocarrier, SU-loaded polymeric micelle (SU-PM) comprised of PEG-
b
-
poly(
lactic acid) (PEG-PLA) copolymer, only reduced toxicity
with no elevated efficacy, despite comparable drug-loading and tumor-targeting
efficiency to SU-MNC.
Improved efficacy of SU-MNC was ascribed to the
carrier-drug synergies with the high-performance carrier of PEG-
EGCG
besides
tumor-targeted delivery.
Eur J Pharm Sci.
2019
Sep
1;137:104972
.
doi
:
10.1016/j.ejps.2019.104972.
Epub
2019 Jun 25.
El-
Kayal
M
1
,
Nasr M
2
,
Elkheshen
S
3
,
Mortada N
2
.
1
Department of Pharmaceutics and
Pharmaceutical Technology, Faculty of Pharmaceutical Sciences and
Pharmaceutical Industries, Future University in Egypt, Cairo, Egypt.
2
Department of Pharmaceutics and
Industrial Pharmacy, Faculty of Pharmacy, Ain Shams University, Egypt.
3
Department of Pharmaceutics and
Pharmaceutical Technology, Faculty of Pharmaceutical Sciences and Pharmaceutical
Industries, Future University in Egypt, Cairo, Egypt. Electronic address:
selkheshen@fue.edu.eg.
Skin carcinogenesis is a common malignancy affecting humans worldwide,
which could benefit from nutraceuticals as a solution to the drawbacks of
conventional skin
cancer
treatment.
(-)-epigallocatechin-3-gallate (
EGCG
) is a
promising nutraceutical in this regard; however, it suffers chemical
instability and low bioavailability resulting in inefficient delivery.
Therefore,
EGCG
encapsulation in
ultradeformable
colloidal vesicular systems, namely: penetration enhancer-containing vesicles
(PEVs),
ethosomes
and
transethosomes
(TEs) for topical administration has been attempted in this study to overcome
the problems associated with the use of free
EGCG
. The prepared vesicles were characterized for their
entrapment efficiency, TEM visualization, chemical compatibility, antioxidant
properties, ex-vivo skin deposition, photodegradation and physical stability
after storage. Most of the prepared vesicles exhibited reasonable skin
deposition and preservation of the inherent antioxidant properties of
EGCG
with good physical stability.
EGCG
-loaded
PEVs and TEs exhibited an inhibitory effect on epidermoid carcinoma cell line
(A431) in addition to reduced tumor sizes in mice, confirmed with
histopathological analysis and biochemical quantification of skin oxidative
stress biomarkers; glutathione, superoxide dismutase and catalase, as well as
lipid
peroxidation.
EGCG
PEVs
succeeded in offering an effective delivery system targeting skin
cancer
,
which is worthy of further experimentation.
J Oral
Pathol
Med.
2019 Aug;48(7):604-610.
doi
: 10.1111/jop.12914.
Epub
2019
Jun 28.
Belobrov
S
1
,
Seers C
1,2
,
Reynolds E
1,2
,
Cirillo N
1,2
,
McCullough M
1,2
.
1
Faculty of Medicine, Dentistry and
Health Science, Melbourne Dental School, The University of Melbourne,
Melbourne, Victoria, Australia.
2
Oral Health Cooperative Research
Centre, Melbourne, Victoria, Australia.
Green tea is heavily consumed on a global basis for its health
benefits. The active ingredient, (-)-epigallocatechin gallate (
EGCG
), is a major polyphenol demonstrated to inhibit the
growth of various non-oral
cancer
cell
lines and interfere
with the carcinogenic process, including downregulation of the epidermal growth
factor receptor (EGFR). Our aim was to determine the phenotypic changes of oral
cancer
cells treated with
EGCG
and concurrently assess the effect on
EGFR expression and activation.
Oral
cancer
cells
(H400 and H357) were treated with 10 µg/mL and 20 µg/mL of
EGCG
for up to 72 hours. Phenotypic
changes were assessed by performing cell proliferation analysis and cell
migration (
Transwell
) assays. Expression of EGFR and
its phosphorylated form (p-EGFR) was determined by Western blotting.
Cell proliferation of both cell lines was significantly reduced at
48hrs when treated with 20 µg/mL
EGCG
. However, after 72 hours of treatment the
effect of
EGCG
on cell proliferation ceased. Treatment
of both cell lines with 10 µg/mL and 20 µg/mL of
EGCG
resulted in significant reduction in
cell migration. Mechanistically, EGFR expression did not change significantly
after treatment with
EGCG
; however, there was a reduction in its
phosphorylated form.
EGCG
transiently inhibits both cell
proliferation and migration of oral cavity
cancer
cells.
This effect
is associated with a decrease in the expression of phosphorylated EGFR. It is
possible that more frequent bursts of
EGCG
could
result in a persistent and sustained
cancer
inhibition,
but this requires further research for clarification.
Oncol Rep.
2019
Jul;42(1):425-435.
doi
: 10.3892/or.2019.7170.
Epub
2019 May 24.
Sun X
1
,
Song J
1
,
Li E
1
,
Geng
H
1
,
Li Y
2
,
Yu D
1
,
Zhong C
2
.
1
Department of Urology, The Second
Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230032, P.R.
China.
2
Department of Nutrition and Food
Safety, Center for Global Health, School of Public Health, Nanjing Medical
University, Nanjing, Jiangsu 211166, P.R. China.
Cancer
stem cells (CSCs) are associated with the
occurrence and metastasis of human malignant tumors, and targeting CSCs is an
important strategy for
cancer
prevention
and overcoming drug resistance. (
‑)‑
Epigallocatechin‑3‑gallate (
EGCG
), a bioactive polyphenol from green tea, has been
studied extensively for its beneficial effects on various tumors including
bladder
cancer
.
However, the mechanism underlying the effect of
EGCG
on bladder CSCs remains poorly
understood. Here, the authors investigated the expression of bladder CSCs
markers including cluster of differentiation (CD)44, CD133, Oct4, ALDH1A1
and Nanog, and their role in the effect of
EGCG
on
bladder CSCs.
EGCG
inhibited
bladder
cancer
tumorspheres
,
downregulated stem cell markers, suppressed the expression of proliferation‑associated
proteins in and promoted the apoptosis of bladder CSCs. The effect of
EGCG
was mediated by the sonic hedgehog
signaling pathway, and upregulation of sonic hedgehog signaling pathway
components attenuated the suppressive effects of
EGCG
.
Taken together, the
results indicated that
EGCG
could
be an important natural compound against bladder CSCs and provide new insights
into the effective molecular targeting of bladder CSCs.
Mol Med Rep.
2019
Aug;20(2):1139-1148.
doi
: 10.3892/mmr.2019.10331.
Epub
2019 Jun 4.
Yoshimura H
1
,
Yoshida H
1
,
Matsuda S
1
,
Ryoke
T
1
,
Ohta
K
1
,
Ohmori
M
1
,
Yamamoto S
1
,
Kiyoshima
T
2
,
Kobayashi M
3
,
Sano K
1
.
1
Department of Dentistry and Oral Surgery,
Unit of Sensory and Locomotor Medicine, Division of Medicine, Faculty of
Medical Sciences, University of Fukui,
Eiheiji
, Fukui
910‑1193, Japan.
2
Laboratory of Oral Pathology,
Division of Maxillofacial Diagnostic and Surgical Sciences, Faculty of Dental
Science, Kyushu University Fukuoka 812‑8582, Japan.
3
Department of Tumor Pathology, Unit
of Pathological Sciences, Division of Medicine, Faculty of Medical Sciences,
University of Fukui,
Eiheiji
, Fukui 910‑1193, Japan.
Oral squamous cell carcinoma (OSCC) is one of the most common
malignant tumors in the oral region. Despite current therapeutic strategies,
the survival rate has not been improved for several decades. Thus, it is
important to develop a novel approach for the treatment of OSCC.
Epigallocatechin‑3‑gallate (
EGCG
) is a major
constituent of green tea and has previously been demonstrated to inhibit the
growth of several types of
cancer
cells.
However, few studies have investigated the effect of
EGCG
on human OSCC cells, especially in
experimental animal models. The aim of the present study was to evaluate the
therapeutic potential of
EGCG
for
targeting human OSCC in vitro and in vivo. In the in vitro
experiments,
EGCG
suppressed
HSC‑3 cell viability in a time‑ and dose‑dependent manner. Cell cycle
analysis revealed that
EGCG
induced
G1 phase arrest of the tumor cells. Apoptosis was examined by Annexin V
and propidium iodide staining, assays of caspase‑3 and -7 activity and
TdT
‑mediated
dUTP
nick end
labeling (TUNEL) staining. Treatment with
EGCG
significantly increased caspase‑3 and
-7 activities, and the percentage of apoptotic cells when compared with control
cells. In the in vivo xenograft experiment on mice,
EGCG
treatment
resulted in a 45.2% reduction in tumor size as compared with the control group
without weight loss. In vivo cell proliferation and apoptosis were
assessed by immunohistochemical Ki‑67 staining and the TUNEL staining. There
were significant differences in Ki‑67 expression between the
EGCG
treatment group and control group, and
the
percentage of apoptotic cells in the
EGCG
treatment
group was significantly greater than that in the control group.
These
results indicated that
EGCG
significantly
inhibited cell proliferation by affecting the cell cycle progression and
apoptosis in vitro and in vivo. These findings suggest that
EGCG
may have clinical
applications as a novel approach to oral‑
cancer
therapy.
PLoS
One.
2019 May 31;14(5
):e
0217676.
doi
: 10.1371/journal.pone.0217676.
eCollection
2019.
Lu CH
1,2
,
Chen WT
1,2
,
Hsieh CH
1,2
,
Kuo
YY
1,2
,
Chao CY
1,2,3
.
1
Department of Physics, Lab for
Medical Physics & Biomedical Engineering, National Taiwan University,
Taipei, Taiwan.
2
Biomedical & Molecular Imaging
Center, National Taiwan University College of Medicine, Taipei, Taiwan.
3
Institute of Applied Physics,
National Taiwan University, Taipei, Taiwan.
Hyperthermia (HT) has shown feasibility and potency as an
anticancer therapy. Administration of HT in the chemotherapy has previously
enhanced the cytotoxicity of drugs against pancreatic
cancer
.
However, the drugs used when conducting these studies are substantially
conventional chemotherapeutic agents that may cause unwanted side effects.
Additionally, the thermal dosage in the treatment of
cancer
cells could also probably harm the
healthy cells. The purpose of this work was to investigate the potential of the
two natural polyphenolic compounds, epigallocatechin gallate (
EGCG
) and chlorogenic acid (CGA), as heat
synergizers
in the thermal treatment of the PANC-1 cells.
Furthermore, we have introduced a unique strategy entitled the thermal
cycling-hyperthermia (TC-HT) that is capable of providing a maximum synergy and
minimal side effect with the anticancer compounds. Our results demonstrate that
the
combination of the TC-HT and the CGA or
EGCG
markedly exerts the anticancer effect
against the PANC-1 cells, while none of the single treatment induced such
changes.
The synergistic activity was attributed to the cell cycle arrest
at the G2/M phase and the induction of the ROS-dependent mitochondria-mediated
apoptosis. These findings not only represent the first in vitro thermal
synergistic study of natural compounds in the treatment of pancreatic
cancer
,
but also highlight the potential of the TC-HT as an alternative strategy in
thermal treatment.
Cancer
Metab
.
2019
May 20;7:4.
doi
: 10.1186/s40170-019-0198-7.
eCollection
2019.
Peeters
TH
#1
,
Lenting
K
#2
,
Breukels
V
1
,
van Lith SAM
1
,
van den Heuvel CNAM
2
,
Molenaar
R
3
,
van
Rooij
A
4
,
Wevers
R
4
,
Span PN
5
,
Heerschap
A
1
,
Leenders
WPJ
2
.
Mutations in isocitrate dehydrogenase 1 (
IDH1
) occur in
various types of
cancer
and
induce metabolic alterations resulting from the
neomorphic
activity that causes production of
D
-2-hydroxyglutarate
(
D-
2-HG) at the expense of α-ketoglutarate (α-KG) and NADPH. To overcome
metabolic stress induced by these alterations,
IDH
-mutated (
IDH
mut
)
cancers utilize rescue mechanisms
comprising pathways in which glutaminase and glutamate dehydrogenase (GLUD) are
involved. We hypothesized that inhibition of glutamate processing with the
pleiotropic GLUD-inhibitor epigallocatechin-3-gallate (
EGCG
)
would not only hamper
D-
2-HG
production, but also decrease NAD(P)H and α-KG synthesis in
IDH
mut
cancers, resulting in increased metabolic
stress and increased sensitivity to radiotherapy.
We performed
13
C-tracing
studies to show that HCT116 colorectal
cancer
cells
with an
IDH1
R132H
knock-in allele depend more on
glutaminolysis
than on glycolysis for the production of
D
-2-HG. We treated HCT116
cells, HCT116-
IDH1
R132H
cells, and HT1080 cells (carrying an
IDH1
R132C
mutation) with
EGCG
and evaluated
D-
2-HG production, cell proliferation
rates, and sensitivity to radiotherapy.
Significant amounts of
13
C from
glutamate accumulate in
D-
2-HG
in HCT116-
IDH1
wt
/R132H
but not in HCT116-
IDH1
wt
/
wt
.
Preventing
glutamate processing in HCT116-
IDH1
wt
/R132H
cells with
EGCG
resulted
in reduction of
D-
2-HG
production. In addition,
EGCG
treatment
decreased proliferation rates of
IDH1
mut
cells and at high doses sensitized
cancer
cells to ionizing radiatio
n. Effects
of
EGCG
in IDH-mutated cell lines were
diminished by treatment with the IDH1
mut
inhibitor AGI-5198.
This work shows that
glutamate can be directly processed into
D-
2-HG and that reduction of
glutamatolysis
may be an effective and promising new
treatment option for
IDH
mut
cancers.
^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^^
Curcumin
https://www.ncbi.nlm.nih.gov/pubmed/?term=curcumin+cancer (hundreds of papers)
J
Gastrointest
Oncol.
2019 Aug;10(4):766-776.
doi
: 10.21037/jgo.2019.03.07.
Hatab
HM
1
,
Abdel Hamid FF
1
,
Soliman AF
1
,
Al-
Shafie
TA
2
,
Ismail YM
3
,
El-
Houseini
ME
4
.
1
Biochemistry Department, Faculty of
Science, Ain Shams University, Cairo, Egypt.
2
Pharmacology and Therapeutics Department,
Faculty of Pharmacy and Drug Manufacturing, Pharos University in Alexandria,
Alexandria, Egypt.
3
Medical Oncology Department,
National
Cancer
Institute, Cairo University, Cairo,
Egypt.
4
Cancer
Biology Department, National
Cancer
Institute, Cairo University, Cairo,
Egypt.
Investigating and evaluating possible alternative therapeutic strategies
to control hepatocellular carcinoma (HCC) is a critical need because of its
high prevalence and being one of the most lethal cancers.
Curcumin
and taurine showed potent anti-tumor
activities in pre-clinical and clinical studies by targeting multiple pathways.
Thus, this study was designed to assess the effect of a combined treatment
consisted of
curcumin
,
piperine
, and
taurine on circulating levels of interleukin-10 (IL-10), and microRNAs miR-141
and miR-21.
Twenty eligible HCC patients administrated an oral dose of 4 g
curcumin
,
40 mg
piperine
, and 500 mg taurine daily for three
successive treatment cycles, each was a 30-day. The level of IL-10 along with
the expression levels of miR-141, and miR-21 were monitored in serum before
starting the treatment and after each cycle. Patients were followed-up for a
period of 24 months.
The combined treatment was able to produce a significant decrease
in the levels of serum IL-10, and miR-21 while it resulted in a non-significant
up-regulation of serum miR-141 expression level. At the end of the follow-up
period, the median overall survival (OS) rate was found to be 17.00 months with
a worse OS in patients with high baseline levels of circulating IL-10 and miR-21
compared to those with low levels. In contrast, a low baseline level of
circulating miR-141 was associated with poor prognosis.
The combined treatment may be able to increase the OS rate by
altering the circulating level of IL-10 and miR-21.
Biomed
Pharmacother
.
2019 Aug 3;118:109278.
doi
: 10.1016/j.biopha.2019.109278. [
Epub
ahead of print]
Jakubek
M
1
,
Kejík
Z
2
,
Kaplánek
R
3
,
Hromádka
R
4
,
Šandriková
V
5
,
Sýkora
D
6
,
Antonyová
V
2
,
Urban M
7
,
Dytrych
P
8
,
Mikula
I
9
,
Martásek
P
10
,
Král
V
11
.
Gastric
cancer
is a common oncological disease. Although enormous
efforts have been expended, possible therapeutic modalities are still limited.
For this reason, new therapeutic approaches and agents are highly requested and
intensively developed. One strategy is the application of natural agents, such
as
curcumin
, with
proven
anticancer effects and low toxicity
for patients. Therefore, this review
discusses the potential application of
curcumin
in
the
therapy of gastric
cancer
and its
potential incorporation in therapeutic regimens. Because one of the largest impediments
for widespread
curcumin
application
is its limited bioavailability (caused mainly by its very low water
solubility), studied strategies (drug delivery systems and
curcumin
derivatization) aimed to solve this obstacle
are discussed in more detail.
Naunyn
Schmiedebergs
Arch
Pharmacol
.
2019
Aug 3.
doi
: 10.1007/s00210-019-01688-1. [
Epub
ahead of print]
Fahmy HM
1
.
1
Biophysics Department, Faculty of
Science, Cairo University, 16 El Zafer Street, Haram, Giza, Egypt.
heba_moh_fahmi@yahoo.com.
In the present study, thymoquinone-loaded liposomes (Lip (TQ)),
curcumin
-encapsulated
liposome (Lip (CUR)), and thymoquinone/
curcumin
-encapsulated
liposome (Lip (TQ + CUR)) in addition to rhodamine-labeled thymoquinone/
curcumin
liposome
(Lip (TQ + CUR + ROD)) were prepared with encapsulation efficiency exceeding
99%. The aim of the present study was to evaluate the effect of the different
prepared formulations either labeled with the fluorescent dye (rhodamine B) or
not on A549 lung
cancer
cells.
Cytotoxicity of different formulations was assessed by MTT assay. Proliferation
of A549 cells was significantly inhibited by the different formulations in a
concentration-dependent manner in 72 h. The Lip (TQ + CUR + ROD)
formulation demonstrated the lowest IC
50
value. To
investigate its mechanism of action on A549 lung
cancer
cells, the Comet assay (for DNA
damage) was done, the measurement of some oxidative stress parameters in
addition to performing inverted fluorescence microscopy imaging. The results of
the present study demonstrated the increased DNA damage, oxidative stress
damage, and cell apoptosis in A549 treated with TQ, CUR, and
rhodamine-encapsulated fluorescent liposome formulation as compared to
untreated cells. The results obtained from the present study demonstrate the
significant role of the TQ/CUR fluorescent liposomes on decreasing the
viability of A549 lung
cancer
cells.
Graphical abstract.
Colloids Surf B
Biointerfaces
.
2019 Jul 29;182:110405.
doi
: 10.1016/j.colsurfb.2019.110405. [
Epub
ahead of print]
Yang R
1
,
Fang XL
1
,
Zhen Q
1
,
Chen QY
2
,
Feng C
3
.
Tumor cells are sensitive to the disturbance of mitochondrial
functions. Attenuation of dysfunctional mitochondria by natural compounds is an
emerging strategy for the recovery of abnormal energy metabolism of
cancer
.
To develop a nano-sized
curcumin
(CUR)
in attenuating the energy metabolism of
cancer
cells,
herein, a coral-shaped nano-transporter DNA-FeS
2
-DA
nanoparticle was synthesized using double-stranded DNA rich in 'GAG' and 'GC'
series as a template and poly-dopamine as an adhesive. CUR was successfully
loaded to DNA-FeS
2
-DA with a molar ratio of ssDNA: CUR of 1:16, forming CUR@DNA-FeS
2
-DA. This
nano-
curcumin
can
readily enter mitochondrion in MCF-7
cancer
cells.
The CUR@DNA-FeS
2
-DA nanocomposite displays desirable photothermal effect and
stability, while its CUR can be released gradually in the weak acid
environment. The expression of both pyruvate kinase M2 and fatty acid synthase
in the MCF-7
cancer
cells
were noticeably inhibited by CUR@DNA-FeS
2
-DA. Given
the controlled release and mitochondria-targeting properties, this CUR@DNA-FeS
2
-DA
nanocomposite is a promising new drug entity for intervening the energy
metabolism of
cancer
cells.
Br J
Pharmacol
.
2019 Aug 1.
doi
:
10.1111/bph.14816. [
Epub
ahead of print]
Lin SR
1
,
Chang CH
1
,
Hsu CF
1,2
,
Tsai MJ
3
,
Cheng H
3
,
Leong MK
4
,
Sung PJ
5
,
Chen JC
6
,
Weng CF
5,7
.
Traditional
chemotherapy is being considered due to hindrances caused by systemic toxicity.
Currently the administration of multiple chemotherapeutic drugs with different
biochemical/molecular targets, known as
combination chemotherapy
, has
attained numerous benefits like
efficacy enhancement and amelioration of
adverse effects th
at has been broadly applied to various
cancer
types. Additionally
, seeking natural-based
alternatives with less toxicity has become more important
. Experimental
evidence suggests that
herbal extracts such as Solanum nigrum and Claviceps
purpurea and isolated herbal compounds (e.g.,
curcumin
, resveratrol, and
matairesinol
) combined with antitumoral drugs have the
potential to attenuate resistance against
cancer
therapy and
to exert chemoprotective actions
. Plant products are not free of
risks: herb adverse effects, including herb drug interactions, should be
carefully considered.
Adv
Healthc
Mater.
2019 Jul
31:e
1900501.
doi
: 10.1002/adhm.201900501. [
Epub
ahead of print]
Wang C
1,2
,
Yu F
1
,
Liu X
1
,
Chen S
1
,
Wu R
1
,
Zhao R
3
,
Hu F
1
,
Yuan H
1
.
Calcium (Ca
2
+
)
hemeostasis
is crucial for the normal function of cellular
biochemistry. The abnormal frequency of Ca
2+
signaling in
cancer
cells
makes them more vulnerable to Ca
2+
modulation than normal cells. Here in this
study, a novel
cancer
-specific therapy by artificially triggering Ca
2+
overload in
cancer
cells
is proposed. The feasibility of this therapy is illustrated by successful
coupling of selective extrusion (Ca
2
+
)
inhibition
effect of
Curcumin
(Cur) and the effective Ca
2+
generating capability of amorphous calcium
carbonate (ACC) into a facilely prepared water responsive phospholipid (PL)-ACC
hybrid platform (PL/ACC-Cur). The obtained results demonstrate that PL/ACC-Cur
can specifically boost the intracellular Ca
2+
concentration to cause Ca
2+
overload and to trigger mitochondria-related
apoptosis in MCF-7 cells while sparing normal hepatocyte (L02), which might be
a promising approach for effective
cancer
therapy.
J Pharm Biomed Anal.
2019 Jun 28;175:112738.
doi
: 10.1016/j.jpba.2019.06.035. [
Epub
ahead of print]
Zhou JL
1
,
Zheng JY
2
,
Cheng XQ
3
,
Xin GZ
2
,
Wang SL
4
,
Xie
T
5
.
Turmeric
(Curcuma longa L,
Zingiberaceae
) rhizomes exhibit
versatile biological activities including the significant anti-
cancer
property. As
an herbal medicine, the therapeutic effects of turmeric may be expressed by
multi-components which have complicated integration effects on multi-targets.
Therefore, having previously found three A549 cell-binding curcuminoids (
curcumin
, Cur;
demethoxycurcumin
,
DMcur
; bisdemethoxycurcumin,
BMcur
)
from turmeric, studies were undertaken in this paper to determine the anti-
cancer
mechanism
and integration effects of these curcuminoids by using chemical markers'
knockout and UHPLC-LTQ Orbitrap MS-based metabolomics. Four
curcuminoid-containing fractions including a mixture of 3 cell-binding
curcuminoids (CE), and three individual curcuminoids with natural proportion in
turmeric were prepared by chemical markers' knockout method. CE, Cur,
DMcur
and
BMcur
fractions showed
significant anti-
cancer
activity on A549 cells. The activities of CE,
Cur and
BMcur
fractions were comparative with the
turmeric crude extract (
TcE
). In the metabolomics
study, CE and three individual curcuminoid fractions changed the expression of
25 metabolites in A549 cells, which were involved in glycerophospholipid
catabolism, sphingolipid metabolism and fatty acid metabolism, etc. Among them,
glycerophospholipid catabolism was disordered greatly in CE group, while
sphingolipid metabolism was suggested to be closely related to
DMcur
and
BMcur
activity.
Furthermore, the metabolomics data showed that three curcuminoids existed
synergistic and antagonistic actions and the use of multi-curcuminoids is more
powerful than use of single curcuminoid on the metabolic alterations of A549
cells.
Rutin
.
https://www.ncbi.nlm.nih.gov/pubmed/?term=rutin+cancer
Endocr
Metab
Immune
Disord
Drug Targets.
2019 Aug 6.
doi
:
10.2174/1871530319666190806122257. [
Epub
ahead of
print]
Khan F
1
,
Pandey P
1
,
Upadhyay TK
2
,
Jafri A
3
,
Jha NK
1
,
Mishra R
4
,
Singh V
4
.
Nowadays the potential therapeutic role of various bioflavonoids
including
Curcumin
,
Luteolin and Resveratrol has currently been well-documented in a vast range of fatal
complications including synaptic failure and cancers. These bioflavonoids are
widely being implemented in the treatment of various cancers as these possess
anti-cancerous, anti-oxidant and anti-inflammatory properties. Moreover, these
are also used as a better alternative to conventional therapies since; these
are non-toxic to cells and having no or least side effects. Notably, the
pertinent therapeutic role of
Rutin
in cervical
cancer
is still unsettled however its
anti-cancerous role has already been reported in other cancers including
prostate and colon
cancer
.
Rutin
(Vitamin P or
Rutoside
) is a polyphenolics flavonoid exhibiting
multi-beneficial roles against several carcinomas.
Despite the evidence for its several biological activities, the
anticancer effects of
Rutin
on human cervical
cancer
(C33A) cells remain to be explored. In
this study, the anticancer potential of
Rutin
was
investigated by employing the key biomarkers such as nuclear condensation
reactive oxygen species (ROS), apoptosis, and changes in mitochondrial membrane
potential (MMP).
Our findings showed that
Rutin
treatment
reduced the cell viability, induced significant increase in ROS production and
nuclear condensation in dose dependent manner. Moreover,
Rutin
provoked apoptosis by inducing decrease in MMP and activation of caspase-3.
Cell cycle analysis further confirmed the efficacy of
Rutin
by showing cell cycle arrest at G0/G1 phase.
Thus, our study is envisaged to open up interests for elucidating
Rutin
as an anti-cancerous agent against cervical
cancer
.
Berberine
https://www.ncbi.nlm.nih.gov/pubmed/?term=berberine+cancer
;
Biol Res.
2019 Jul
18;52(1):37.
doi
: 10.1186/s40659-019-0243-6.
Liu L
1
,
Fan J
2
,
Ai G
1
,
Liu J
1
,
Luo N
1
,
Li C
1
,
Cheng Z
3
.
Piperine
.
https://www.ncbi.nlm.nih.gov/pubmed/?term=piperine+cancer
;
J
Gastrointest
Oncol.
2019 Aug;10(4):766-776.
doi
: 10.21037/jgo.2019.03.07.
Hatab
HM
1
,
Abdel Hamid FF
1
,
Soliman AF
1
,
Al-
Shafie
TA
2
,
Ismail YM
3
,
El-
Houseini
ME
4
.
Etc.
Suloraphane
.
https://www.ncbi.nlm.nih.gov/pubmed/?term=sulforaphane+cancer
;
Phytomedicine.
2019 Jul
29;63:153058.
doi
: 10.1016/j.phymed.2019.153058. [
Epub
ahead of print]
Chen L
1
,
Chan LS
1
,
Lung HL
1
,
Yip TTC
2
,
Ngan RKC
2
,
Wong JWC
1
,
Lo KW
3
,
Ng WT
4
,
Lee AWM
5
,
Tsao GSW
6
,
Lung ML
5
,
Mak
NK
7
.
Am J
Cancer
Res.
2019 Jun 1;9(6):1172-1182.
eCollection
2019.
Islam A
1
,
Yang YT
1
,
Wu WH
1
,
Chueh
PJ
1,2,3
,
Lin MH
4,5
.
Quercetin. https://www.ncbi.nlm.nih.gov/pubmed/?term=quercetin+cancer ; dozens
Food
Funct
.
2019 Aug 8.
doi
:
10.1039/c9fo01168d. [
Epub
ahead of print]
Pang B
1
,
Xu X
1
,
Lu Y
1
,
Jin
H
1
,
Yang R
1
,
Jiang C
1
,
Shao D
1
,
Liu Y
2
,
Shi J
1
.
Am J Chin Med.
2019;47(4):841-863.
doi
: 10.1142/S0192415X19500447.
Epub
2019 May 16.
Tsai YH
1
,
Lin JJ
2,3
,
Ma YS
4,5
,
Peng SF
1
,
Huang AC
6
,
Huang YP
7
,
Fan MJ
8
,
Lien JC
9
,
Chung JG
1,8
.
Biomolecules.
2019
May 6;9(5).
pii
: E174.
doi
:
10.3390/biom9050174.
Kashyap D
1
,
Garg VK
2
,
Tuli HS
3
,
Yerer
MB
4
,
Sak
K
5
,
Sharma AK
6
,
Kumar M
7
,
Aggarwal V
8
,
Sandhu SS
9
.
Cancer
Epidemiol
Biomarkers Prev.
2019
Aug 6.
pii
: cebp.1075.2018.
doi
:
10.1158/1055-9965.EPI-18-1075. [
Epub
ahead of print]
Zhang W
1
,
Wang J
2
,
Gao J
3
,
Li HL
2
,
Han LH
2
,
Lan Q
4
,
Rothman N
4
,
Zheng W
5
,
Shu XO
5
,
Xiang YB
6
.
Our
study suggests for the first time that urinary excretion of
genistein
may
be associated with reduced risk of liver
cancer
in women.
Arch Med Sci.
2019
Jul;15(4):1001-1009.
doi
: 10.5114/aoms.2018.78742.
Epub
2018 Oct 3.
Zhang Q
1
,
Bao J
2
,
Yang J
1
.
Folate https://www.ncbi.nlm.nih.gov/pubmed/?term=folate+cancer ; hundreds
J
Prev
Med Public Health.
2019 Jul;52(4):205-213.
doi
: 10.3961/jpmph.19.020.
Epub
2019 Jul 2.
Alpha Carotene https://www.ncbi.nlm.nih.gov/pubmed/?term=alpha+carotene+cancer ;
Asian Pac J
Cancer
Prev.
2018 Nov 29;19(11):3251-3256.
Dutta S
1
,
Surapaneni
BK
,
Bansal A
.
Our
results suggest that a combination of α-and β-carotene may provide a novel
strategy for prevention and treatment of esophageal and upper aero digestive
tract
cancer
in humans.
Beta Carotene https://www.ncbi.nlm.nih.gov/pubmed/?term=beta+carotene+cancer ;
Antioxidants (Basel).
2019
Jul 19;8(7).
pii
: E229.
doi
:
10.3390/antiox8070229.
Elvira-
Torales
LI
1,2
,
García-Alonso J
3
,
Periago-Castón
MJ
4
.
he
consumption of carotenoids has beneficial effects on health, reducing the risk
of certain forms of
cancer
, cardiovascular diseases, and macular degeneration,
among others.
PUFAs, DHA . https://www.ncbi.nlm.nih.gov/pubmed/?term=PUFAs+cancer ;
J Lipid Res.
2019
Jul 25.
pii
: jlr.M090712.
doi
:
10.1194/jlr.M090712. [
Epub
ahead of print]
Yamada H
1
,
Hakozaki
M
2
,
Uemura
A
2
,
Yamashita T
3
.
We
found that DHA interacts with Rack1 and represses melanoma cell proliferation
by suppressing PKC signaling
PLoS
One.
2019 Jul 17;14(7
):e
0219822.
doi
: 10.1371/journal.pone.0219822.
eCollection
2019.
Bratton BA
1
,
Maly
IV
1
,
Hofmann WA
1
.
Our
data show that the hormone-dependent cells are comparatively insensitive to
various
PUFAs
, at the same time as the growth and viability of
hormone-independent cells lines are strongly inhibited by most of the
tested
PUFAs
, whether n-3 or n-6. We
speculate that this difference may be at least partially responsible for the
observed effects of specific dietary lipids in prostate
cancer
. The new data strengthen the case for dietary
intervention as part of potential new therapeutic strategies seeking to impede
prostate
cancer
progression.