Saturday, 2 December 2017

Herbal Therapy: Green Tea (-)-Epigallocatechin-3-O-Gallate (EGCG) For Prevention and Treatment of Melanoma

Kyle J. Norton (Scholar, Master of Nutrients, All right reserved)


Green tea may have a profound and sustainable effect in reduced risk and treatment of melanoma, some scientists suggested.

Melanoma, is a medical condition characterized by irregular cell growth of  pigment-containing cells known as melanocytes. At the later stage, the cancerous cells may travel a distance away to infect other healthy organs and tissues.
According to the study, approximately 7,200 Canadians will be diagnosed with melanoma skin cancer.

Green tea, a precious drink processes numbers of health benefit known to almost everyone in Asia and Western world. However, as yin in nature herbal medicine or food, long term injection of large amounts may obstruct the balance of yin-yang, induced "yin excessive syndrome" or "yang vacuity syndrome" including weaken immunity and painful case of GERD,... according to traditional Chinese medicine's Yin-Yang theory.

In the review of literature published online, green tea bioactice EGCG significantly inhibited the growth, migration and invasion of melanoma cells through numbers of mechanism.

Gene implications in initiated cancer development and cancerous cells proliferation have gone through extensive research, particularly in melanoma.

In melanoma, green tea biactice EGCG demonstrated a significant effect in knockdown gene over expression (TRAF6) in reduced migration and invasion of melanoma.

TRAF6 is a protein with function in activation of IkappaB kinase (IKK) in response to inflammation.

In fact, green tea biactive EGCG directly bind to TRAF6 in melanoma in attenuated the interaction of
between TRAF6 and UBC13(E2) in activated the protein (IkappaB kinase (IKK)) in production of pro inflammatory cytokins.

The ubiquitin-conjugating enzyme(UBC13(E2)) are essential in activation protein (NF- kappa B) in controls transcription of DNA, cytokine production and cell survival.

Furthermore, the phytochemicals also suppressed the TRAF6 E3 ubiquitin ligase activity of the tumor generated by TRAF6 in regulation of important biological processes, particularly, in cell division and for the survival of the tumors.

Additionally, green tea biactice EGCG also regulated the gene expression of proteins (IκBα and p-TAK1 e) in modulation and inactivated NF-κB-directed gene expression of inflammation, immunity, cell proliferation, differentiation, and survival in melanoma.

Dr. Zhang J, the lead author said, " EGCG is a novel E3 ubiquitin ligase inhibitor that could be used to target TRAF6 for chemotherapy or the prevention of melanoma".


Other researchers in focus of Green tea polyphenol (-)-epigallocatechin-3-O-gallate (EGCG) effect in attenuated and treatment of melanoma in the gene implication via MicroRNAs (miRNAs, non-coding RNAs involved in various biological processes by regulating their target genes) also indicated that

Green tea polyphenol (-)-epigallocatechin-3-O-gallate (EGCG) inhibited melanoma tumor growth by activating 67-kDa laminin receptor (67LR) signaling which has an function in down regulated tumor cell proliferation and tumor formation by inducing apoptosis.

The bioactive compound also up-regulated miRNA-let-7b expression in induced tumor suppressor function in decrease function of 67LR in enhanced invasive and metastatic melanoma cells.

Indeed, green tea EGCG-also displayed a significant effect in promote function of let-7b in altering the traits,of malignant cell in melanoma through regulating the expression of HMGA2.with action as DNA transcriptional regulator.

Green tea EGCG. also induced expression of  let-7b  in inhibitions of oncoproteins and activation of tumor suppressor via tumor-over expressed 67LR in activation of PP2A, a tumor suppressor. through adenylate cyclase/cAMP pathway in cell communication.

In compared the effects of TNF-related apoptosis-inducing ligand (TRAIL), a protein with function in in induced tumor cells apoptosis. and green tea bioactive EGCG for treatment of groups of melanoma.
In A375 melanoma cell line, TRAIL application group demonstrated a strong effect in inhibition with apoptosis rate was 11.8% at dose of 150ng/mL in compared to green tea EGCG treatment group of 5%-7% .

Interestingly, in combined TRAIL and green tea EGCG treatment groups, the inhibited rate increased sufficiently to 48.9 - 59.1%

Further analysis also found that EGCG effective in treatment of melanoma was attributed to activity of caspase-3 rather than caspase-8 in mediation of programmed cell death (apoptosis).

The findings suggest that by blocking the sequence of gene expression of tumor, green tea polyphenol (-)-epigallocatechin-3-O-gallate (EGCG) may be considered as an adjunct combined with TRAIL for prevention and treatment of melanoma.



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Author Biography
Kyle J. Norton (Scholar, Master of Nutrients, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published on line, including world wide health, ezine articles, article base, healthblogs, selfgrowth, 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 international journal Pharma and Bio science, ISSN 0975-6299.

Sources
(1) Epigallocatechin-3-gallate(EGCG) suppresses melanoma cell growth and metastasis by targeting TRAF6 activity by Zhang J1,2, Lei Z1,2, Huang Z3, Zhang X1,2, Zhou Y1,2, Luo Z1,2, Zeng W1,2, Su J1,2, Peng C1,2, Chen X1,2.(PubMed)
(2) EGCG enhances TRAIL-mediated apoptosis in human melanoma A375 cell line by Shen Q1, Tian F, Jiang P, Li Y, Zhang L, Lu J, Li J.(PubMed)
(3) Epigallocatechin-3-O-gallate up-regulates microRNA-let-7b expression by activating 67-kDa laminin receptor signaling in melanoma cells by Yamada S1, Tsukamoto S1, Huang Y1, Makio A1, Kumazoe M1, Yamashita S1, Tachibana H1.(PubMed)

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