Green tea may have a therapeutic and positive effect in reduced risk and treatment of esophageal cancer, some scientists suggested.
Green tea, a precious drink processes a number of health benefits known to almost everyone in Asia and the Western world. However, as yin in nature herbal medicine or food, long-term injection of large amounts may obstruct the balance of yin-yang, inducing "excessive yin syndrome" or "yang vacuity syndrome" including weakened immunity and painful case of GERD,... according to traditional Chinese medicine's Yin-Yang theory.
Esophageal cancer is a medical condition characterized by irregular cell growth in the tissues of the esophagus. At the later stage, the cancerous cells may travel a distance away to invade other healthy tissues and organs.
According to statistics, 2,300 Canadians will be diagnosed with esophageal cancer in 2017.
In the review of the literature published online, green tea efficacy in the treatment of human esophageal squamous cell carcinoma was expressed in a number of mechanisms.
In esophageal cancer cell lines Eca109 and Ec9706, injection of green tea EGCG plus chemo drug adriamycin (ADM) after 24 hours displayed a significantly increased cellular apoptosis.
According to the flow cytometry assay, the application induced the elevation of ROS and ADM concentration in the production of toxicity to counter the reaction of tumor cell in diminished expression of mitochondrial membrane potential and ABCG2 protein to induced apoptosis.without harming to healthy cells.
ABCG2 protein expression plays a major role in multi-drug resistance, produced by tumor cells to accounter reaction to chemo-medicine.
Mitochondrial membrane potential is a central intermediate in oxidative energy metabolism, the deceased levels caused by toxicity ROS may result in energy deletion and subsequently, cause cell death.
Further observation also indicated that EGCG inhibited the growth of Eca109 and Ec9706 cells through ameliorating the anti-apoptotic bcl-2 protein expression and promoted bax and caspase-3 protein expressions with functions in induced apoptosis in a dose- and time-dependent manner.
BCL2 family members form hetero- or homodimers and play an important anti-apoptotic protein.
Caspase-3 protein. plays a central role in the execution phase of cell apoptosis.
BAX gene. BAX is a member of the Bcl-2 gene family. plays an important role in the mediation of cell death by apoptosis.
Compared to ADM treatment alone, the Eca109/ABCG2 multi-drug resistance cancer cells, rate of apoptosis and ADM concentration were significant higher anid levels of mitochondrial membrane potential and ABCG2 expression were lower.
In other word, injection of green tea plus ADM was more effective in induced cells death in Eca109/ABCG2 multi-drug resistance cancer cells with expression ROS and ADM in enhanced elevation cytotoxity activity in compared to ADM treatment alone.
After taking into account other confounders, Dr, Liu L the lead author said, " EGCG inhibited cell growth and induced esophageal cancer cell apoptosis. It reduced the bcl-2 protein expression and increased the bax and caspase-3 protein expression. EGCG reversed multi-drug resistance by reducing ABCG2 expression and increasing the anticancer drug concentration in cancer cells".
In esophageal squamous cell carcinoma, application of Epigallocatechin-3-gallate (EGCG) without ADM measured by flow cytometry assay after 24 hours also inhibited cancer site proliferation by increased expression of ROS to attenuate mitochondrial membrane potential function in energy metabolism and caspase-3 protein to cause malignant cellular apoptosis, in a dose and time-dependent manner.
In the examine the PCR-TRAP argentation analysis during the experiment, EGCG was also demonstrated to inhibit the viability of Eca109 and Ec9706 cells by suppressing cancer cells in alternated DNA transcript through telomerase activity.
More interestingly, the continuation of the study of epigallocatechin-3-gallate (EGCG) on the human esophageal cancer cell line ECa109 also discover that EGCG demonstrated a decrease of cancer cell viability but a substantial rate of apoptosis by increased expression of p16 gene demethylation in induced cancer cell cycle arrest and apoptosis, level p16 mRNA expression in suppressed tumor progression of invasive and aggressive behavior. and p16 protein expression in promoted tumor suppressible activity, in a dose- and time-dependent manner.
P16 gene demethylation plays an important role in cell cycle arrest and apoptosis. gene alternation was found in several types of cancer.
A low level of p16 mRNA expression is associated with the progression of cancer with malignant and aggressive behavior.
Abnormalities of the p16 gene and loss of p16 protein expression may be related to the pathogenesis and development of some cancers.
Taken together, green tea with an abundance of phytochemical Epigallocatechin-3-gallate (EGCG) may be considered as an adjunct therapy to combine with standard chemo-medicine in reduced risk and treatment of esophageal cancer.
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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 online, including worldwide health, ezine articles, article base, healthblogs, 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) Epigallocatechin-3-gallate promotes apoptosis and reversal of multidrug resistance in esophageal cancer cells by Liu L1, Ju Y2, Wang J3, Zhou R3. (PubMed)
(2) Epigallocatechin-3-gallate suppresses cell proliferation and promotes apoptosis in Ec9706 and Eca109 esophageal carcinoma cells by Liu L1, Zuo J1, Wang G1.(PubMed)
(3) Epigallocatechin-3-gallate inhibits growth and induces apoptosis in esophageal cancer cells through the demethylation and reactivation of the p16 gene by Meng J1, Tong Q2, Liu X2, Yu Z3, Zhang J3, Gao B3. (PubMed)
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