Abstract
Green tea and its major bioactive component, (−)-epigallocatechin gallate (EGCG), possess diverse biological properties, particularly antiproliferation, antimetastasis, and apoptosis induction. Many studies have widely investigated the anticancer and synergistic effects of EGCG due to the side effects of conventional cytotoxic agents. This review summarizes recent knowledge of underlying mechanisms of EGCG on protective roles for endometrial, breast, and ovarian cancers based on both in vitro and in vivo animal studies. EGCG has the ability to regulate many pathways, including the activation of nuclear factor erythroid 2-related factor 2 (Nrf2), inhibition of nuclear factor-κB (NF-κB), and protection against epithelial–mesenchymal transition (EMT). EGCG has also been found to interact with DNA methyltransferases (DNMTs) and histone deacetylases (HDACs), which affect epigenetic modifications. Finally, the action of EGCG may exert a suppressive effect on gynecological cancers and have beneficial effects on auxiliary therapies for known drugs. Thus, future clinical intervention studies with EGCG will be necessary to more and clear evidence for the benefit to these cancers.
Highlights
Green tea, derived from the Camellia sinensis plant, is the most popular beverage in East Asia
Current research revealed that epigallocatechin gallate (EGCG) with chemical modification, such as polymeric nanogels with matching small interfering RNA, improved the sensitization involved with chemotherapy [8]
The treatment of Ishikawa cells with EGCG resulted in extracellular signal-regulated kinase (ERK) signaling inhibition, including P38, jun N-terminal kinase (JNK), c-jun, and c-fos, and proliferation marker downregulation of estrogen receptor α (ERα), progesterone receptor (PR), proliferating-cell nuclear antigen (PCNA), and cyclin D1 [28]
Summary
Green tea, derived from the Camellia sinensis plant, is the most popular beverage in East Asia. A number of high-risk factors in endometrial cancers are excess exposure to estrogen, late onset of menopause, postmenopausal hormone replacement therapy, obesity, and inflammatory environments [16]. It is suggested that the surface epithelial cells are the primary locus for ovarian cancer and divide into a number of different epithelial types, including serous, endometrioid, mucinous, and clear-cell carcinomas [22]. Some factors, such as incessant ovulation, hormonal stimulation, oncogenes, tumor-suppressor genes, growth factors, and chronic inflammation, contribute to the tumorigenesis or etiology of ovarian cancer [23]. We present and summarize here the anticancer effects of EGCG on gynecological cancers for further study
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