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- Title
Epigallocatechin gallate inhibits the growth of MDA‑MB‑231 breast cancer cells via inactivation of the β‑catenin signaling pathway.
- Authors
ON‑YU HONG; HYE‑YEON JANG; JONG‑SUK KIM; EUN‑MI NOH; YOUNG‑RAE LEE; BYOUNG KIL LEE; SUNG HOO JUNG; HYUN JO YOUN
- Abstract
Epigallocatechin gallate (EGCG), a major constituent of green tea, has potential as a treatment for a variety of diseases, including cancer. EGCG induces apoptosis and inhibits tumorigenesis through multiple signaling pathways in breast cancer cells. β‑catenin signaling modulators could be useful in the prevention and therapy of breast cancer. However, the precise anticancer effect of EGCG through the β‑catenin signaling pathway in breast cancer is unclear. The present study investigated the association between β‑catenin expression and clinicopathological factors of breast cancer patients, and the effect of EGCG on β‑catenin expression in breast cancer cells. β‑catenin expression was analyzed according to the clinicopathological factors of 74 patients with breast cancer. All patients were females diagnosed with invasive ductal carcinoma. Western blot analysis revealed that β‑catenin was expressed at higher levels in breast cancer tissue than in normal tissue. β‑catenin expression was associated with lymph node metastasis (P=0.04), tumor‑node‑metastasis stage (P=0.03) and estrogen receptor status (P<0.01). EGCG decreased MDA‑MB‑231 cell viability and significantly downregulated the expression of β‑catenin, phosphorylated Akt and cyclin D1. Remarkably, additive effects of LY294002 and wortmannin, two phosphatidylinositol‑3 kinase inhibitors, were observed. The present results suggest that EGCG inhibits the growth of MDA‑MB‑231 cells through the inactivation of the β‑catenin signaling pathway. Based on these promising results, EGCG may be a potential treatment for triple negative breast cancer patients.
- Subjects
BREAST cancer; CATENINS; PROTEIN expression; EPIGALLOCATECHIN gallate; CARCINOMA in situ; CELL survival; CANCER cell growth; THERAPEUTICS; PREVENTION
- Publication
Oncology Letters, 2017, Vol 14, Issue 1, p441
- ISSN
1792-1074
- Publication type
Article
- DOI
10.3892/ol.2017.6108