In vitro mechanism of action for the cytotoxicity elicited by the combination of epigallocatechin gallate and raloxifene in MDA-MB-231 cells.

The anticancer effects elicited by epigallocatechin gallate (EGCG) are well established in various models of cancer, while raloxifene is as an established selective estrogen receptor modulator (SERM), which is not yet clinically utilized for the treatment of breast cancer. Previous study from this laboratory has demonstrated that the combination of EGCG (25 microM) and raloxifene (4 microM) elicits a strong cytotoxic response in MDA-MB-231 human breast cancer cells, which lack the estrogen receptor (ER) and erbB-2/ Her-2 receptor. This study was therefore designed to probe the mechanism underlying this cytotoxic response, with an emphasis on determining how the combination treatment influenced the total expression and phosphorylation of key signaling proteins.

Sex-specific differences in CYP450 isoforms in humans.

Background: The activity of various CYP isoforms is critical for maintaining the clinical effectiveness of many medications. Therefore, determining the sex-dependent activity of clinically relevant CYP families is highly important for optimal therapeutic effectiveness.

Objective: This review examined the sex-dependent activity of CYP3A, CYP1A2, CYP2D6, CYP2C9, CYP2C19 and CYP2E1.

The combination of raloxifene and epigallocatechin gallate suppresses growth and induces apoptosis in MDA-MB-231 cells.

Previous studies have demonstrated that raloxifene induces apoptosis in a variety of cancer cell lines. We aimed to determine if this effect was enhanced by combining raloxifene with epigallocatechin gallate (EGCG). Results demonstrated that EGCG (25 microM) and raloxifene (1-5 microM) produced enhanced cytotoxicity toward MDA-MB-231 breast cancer cells compared to either drug alone following 7 days of treatment.

The combination of epigallocatechin gallate and curcumin suppresses ER alpha-breast cancer cell growth in vitro and in vivo.

Both epigallocatechin gallate (EGCG) and curcumin have shown efficacy in various in vivo and in vitro models of cancer. This study was designed to determine the efficacy of these naturally derived polyphenolic compounds in vitro and in vivo, when given in combination. Studies in MDA-MB-231 cells demonstrated that EGCG + curcumin was synergistically cytotoxic and that this correlated with G(2)/M-phase cell cycle arrest.

Potential mechanisms for the synergistic cytotoxicity elicited by 4-hydroxytamoxifen and epigallocatechin gallate in MDA-MB-231 cells.

Potential mechanisms for the synergistic cytotoxicity elicited by epigallocatechin gallate (EGCG) (25 microM) and 4-hydroxytamoxifen (4-OHT) (1 microM) in MDA-MB-231 human breast cancer cells were investigated. The role of apoptosis was determined using chromatin condensation and Annexin-V staining. Condensed chromatin was visible following 24 h of combination treatment while flow cytometry experiments demonstrated that apoptosis was 2-fold greater following 36 h of combination treatment compared to EGCG.

Role of epigallocatechin gallate (EGCG) in the treatment of breast and prostate cancer.

Green tea and its major constituent epigallocatechin gallate (EGCG) have been extensively studied as a potential treatment for a variety of diseases, including cancer. Epidemiological data have suggested that EGCG may provide protective effects against hormone related cancers, namely breast or prostate cancer. Extensive in vitro investigations using both hormone responsive and non-responsive cell lines have shown that EGCG induces apoptosis and alters the expression of cell cycle regulatory proteins that are critical for cell survival and apoptosis.