Endometrial cancer is a medical condition characterized by cell growth uncontrollably in the endometrium. At the late stage, the cancerous cell may travel a distance away from the original site to infect other organs and tissues.
In the review of research papers online, the effects of green tea polyphenol (-)-epigallocatechin-3-gallate (EGCG) in inhibition of endometrial cancer were expressed in various aspects.
In the experiment of green tea bioactive compound against the progression of tumor xenografts of human endometrial cancer, (-)-epigallocatechin-3-gallate EGCG demonstrated a significant effect in reduced risk of endometrial cancer development through the bioactive chemicals anti-tumor angiogenesis properties.
In fact, the anti-cancer active compound efficacy was attributed to the modulation of expression of vascular endothelial growth factor A (VEGFA) protein in the established new vessel to stimulate the onset of cancer and cancer cell proliferation and HIF-1 functions in the activated transcription of many genes, in regulated cellular and systemic homeostatic response to external changes to tumor growth.
Furthermore, application of EGCG also suppressed responses of chemokine (C-X-C motif) ligand 12 (CXCL12) in the expression of multiple physiological processes, in promoted invasion and metastasis of tumor cells in connected tissues of the uterine mucosa (endometrium), thus reducing the infiltration of VEGFA-expressing tumor-associated macrophages (TAMs) in supplying rapidly growing malignant tissues with essential nutrients and oxygen.
Additionally, further analysis also insisted that EGCG restricted secretion of vascular endothelial growth factor A (VEGFA) is initiated endometrial cancer growth by inhibiting the function of PI3K/AKT/mTOR/HIF1α pathway in regulated many cellular processes, including cell survival, proliferation, and growth.
After taking account of all findings, treatment with EGCG reduced the risk of endometrial cancer onset may be a result of EGCG-suppressed secretion in both fronts including decreased cancer cell-secreted VEGFA but inhibited TAM-secreted VEGFA in endometrial cancer progression.
Further differentiation, also showed that green tea polyphenol (-)-epigallocatechin-3-gallate reduced cancer expansion by suppressing the expression of proliferation markers which acts indirectly to stimulate endometrial epithelial proliferation in estrogen receptor α, progesterone receptor, proliferating cell nuclear antigen, and cyclin D1
The overexpression of cyclin D1 has been linked to the development and progression of cancer.
Proliferating cell nuclear antigen is a protein with function in cell cycle regulation and/or DNA replication and is important for both DNA synthesis and DNA repair.
Importantly, the inhibition of EGCG also decreased the activation of ERK, the extracellular signal-regulated kinases protein in cancer cell division, and the down-expression of transcription factors fos and jun, the cellular immediate-early genes in induced transient cancer cell division and differentiation processes.
The function of EGCG in reduced risk of endometrial cancer is also expressed through Bcl-2-associated X protein, cleavage of caspase-3, and poly(ADP-ribose) polymerase actions in the induction of cancer cell apoptosis and suppression of antiapoptotic protein Bcl-2 (B-cell lymphoma 2).
Bcl-2-associated X is a protein with the function of anti- or pro-apoptotic regulators involved in a wide variety of cellular activities.
B-cell lymphoma 2, a family protein with function in the regulation of cell apoptosis.
Cleavage of caspase-3 also is known as a critical executioner of apoptosis,
Poly(ADP-ribose) polymerase is a protein with function involved in a number of cellular processes, including programmed cell death.
Implicitly, the application of EGCG also increased the production of free radical expression in initiating the cytotoxicity effect by reduced levels of antioxidant glutathione levels and activated the p38 in cancer cells death without inducing toxicity to normal cells
P38 mitogen-activated protein kinases (MAPKs) are activated by a wide range of cellular stresses as well as in response to inflammatory cytokines involved in cell differentiation, apoptosis, and autophagy.
Indeed, according to a systematic review of the literature published on the database of PubMed, Embase, Cochrane Library, and China Biological Medicine Database upto February 2, 2015, researchers indicated that green tea consumption was associated with a reduced risk of EC with a relative risk of .78 and each additional cup of green tea consumed per day decreased risk of developing EC by 11%.
Particularly, the intake of green tea associated with attenuated risk of endometrial cancer was 84.33% compared to 5.07 % of black tea.
Taken together, green tea and its polyphenol (-)-epigallocatechin-3-gallate EGCG may be considered a functional food used in conjunction with standard therapy in reduced risk and treatment of endometrial cancer.
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Author Biography
Kyle J. Norton, Master of Nutrition
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, best before it's news, the Karate GB Daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as the international journal Pharma and Bio Science, ISSN 0975-6299.
Sources
(1) Green tea, black tea consumption and risk of endometrial cancer: a systematic review and meta-analysis by Zhou Q1, Li H2, Zhou JG3, Ma Y4, Wu T5, Ma H6.(PubMed)
(2) A prodrug of green tea polyphenol (-)-epigallocatechin-3-gallate (Pro-EGCG) serves as a novel angiogenesis inhibitor in endometrial cancer by Wang J1, Man GCW2, Chan TH3, Kwong J1, Wang CC4.(PubMed)
(3) (-)-Epigallocatechin-3-gallate induces apoptosis in human endometrial adenocarcinoma cells via ROS generation and p38 MAP kinase activation by Manohar M1, Fatima I, Saxena R, Chandra V, Sankhwar PL, Dwivedi A.(PubMed)
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