Epigallocatechin-3-gallate promotes apoptosis and expression of the caspase 9a splice variant in PC3 prostate cancer cells

Hagen, R; Chedea, Veronica Sanda; Mintoff, Christopher; Bowler, Elizabeth; Morse, Hannah; Ladomery, Michael

doi:10.3892/ijo.2013.1920

Cited by 45 publications

(45 citation statements)

References 33 publications

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“…It is used to treat many types of solid cancer, such as ovary, bladder, lung and colorectal cancers. 16 However, the efficacy of cisplatin therapy for metastatic bladder cancer is limited because of intrinsic or acquired drug resistance. 17,18 Therefore, combination therapy based on the synergistic effect between drugs has been used to overcome such drug resistance.…”

Section: Discussionmentioning

confidence: 99%

Synergistic Antitumor Effect of Triptolide and Cisplatin in Cisplatin Resistant Human Bladder Cancer Cells

Byun²,

Lee³

et al. 2015

Journal of Urology

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Section: Discussionmentioning

confidence: 99%

Synergistic Antitumor Effect of Triptolide and Cisplatin in Cisplatin Resistant Human Bladder Cancer Cells

Byun²,

Lee³

et al. 2015

Journal of Urology

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“…Epidemiological investigations and experimental studies have shown that green tea has chemopreventive effects for a wide range of malignancies, including lung, stomach, breast, prostate, pancreatic, ovarian, liver, colorectal and skin cancer (1)(2)(3)(4)(5)(6)(7)(8)(9)(10). Mechanistic studies indicate that EGCG, the major component of green tea, appears to be the primary active ingredient responsible for its biological effects.…”

Section: Introductionmentioning

confidence: 97%

Epigallocatechin gallate inhibits the growth of human lung cancer by directly targeting the EGFR signaling pathway

Cui

Gao

et al. 2013

Oncology Reports

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Epigallocatechin gallate (EGCG), the major biologically active compound in green tea, is a well-known chemoprevention agent. Although several reports have shown that EGCG exerts its anticancer activity by targeting specific cell signaling pathways, the underlying molecular mechanism(s) are only partially understood. In the present study, we report that EGCG had a profound antiproliferative effect on human lung cancer cells. EGCG inhibited anchorage-independent growth and induced cell cycle G0/G1 phase arrest. The mechanism underlying EGCG antitumor potency was mainly dependent on suppression of the EGFR signaling pathway. Short-term EGCG exposure substantially decreased EGF-induced EGFR, AKT and ERK1/2 activation. Moreover, long-term EGCG treatment not only inhibited total and membranous EGFR expression, but also markedly attenuated EGFR nuclear localization and expression of the downstream target gene cyclin D1, indicating that EGCG treatment suppressed EGFR transactivation. Additionally, knockdown of EGFR in lung cancer cells decreased their sensitivity to EGCG. Thus, inhibition of the EGFR signaling pathway may partly contribute to the anticancer activity of EGCG.

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“…Epigallocatechin-3-gallate (EGCG) is a water-soluble catechin, which suppresses the multiplication of cancer cells and induces apoptosis (3)(4)(5). EGCG suppressed adhesion and invasion of hepatocarcinoma cells through antioxidant activity (6).…”

Section: Introductionmentioning

confidence: 99%

Epigallocatechin-3-gallate inhibits cell growth, induces apoptosis and causes S phase arrest in hepatocellular carcinoma by suppressing the AKT pathway

Shen

Zhang

Yan

et al. 2014

International Journal of Oncology

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Abstract. Epigallocatechin-3-gallate (EGCG) has been shown to inhibit the growth and induce apoptosis of certain cancer cells. The aim of this study was to determine the role of EGCG in hepatocellular carcinoma (HCC) and the underlying mechanism(s) thereof. MTT assay was used to determine the cell growth inhibition by EGCG. Apoptosis induced by EGCG was investigated by both AO/EB staining and flow cytometry. The cell cycle distribution was analyzed by flow cytometry. The mRNA levels of the AKT pathway were analyzed by quantitative PCR. The expression of AKT and its phosphorylation at Ser473 were detected by western blotting. The IC 50 of EGCG at 48 h for HepG2, SMMC7721 and SK-hep1 cells were 74.7, 59.6 and 61.3 µg/ml, respectively. Significantly higher proportion of SMMC7721 cells entered the S phase upon treatment with EGCG for 48 h compared with control cells. EGCG decreased the mRNA levels of PI3K, AKT and NF-κB. The protein levels of AKT decreased and its phosphorylation at Ser473 was downregulated with EGCG treatment. EGCG inhibited growth by affecting the cell cycle and induced apoptosis in different HCC cells by downregulating PI3K/ AKT activity. The results suggest the potential of EGCG as an anticancer agent in the prevention or treatment of HCC.

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Epigallocatechin-3-gallate promotes apoptosis and expression of the caspase 9a splice variant in PC3 prostate cancer cells

Cited by 45 publications

References 33 publications

Synergistic Antitumor Effect of Triptolide and Cisplatin in Cisplatin Resistant Human Bladder Cancer Cells

Synergistic Antitumor Effect of Triptolide and Cisplatin in Cisplatin Resistant Human Bladder Cancer Cells

Epigallocatechin gallate inhibits the growth of human lung cancer by directly targeting the EGFR signaling pathway

Epigallocatechin-3-gallate inhibits cell growth, induces apoptosis and causes S phase arrest in hepatocellular carcinoma by suppressing the AKT pathway

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