Triptolide inhibits MCF‐7 cell growth via estrogen receptor‐α‐related pathways (657.5)

Triptolide, a diterpenoid triepoxide from the traditional Chinese medicinal herb Tripterygium wilfordii Hook. f., is a potential treatment for autoimmune diseases as well a possible anti‐tumor agent. Our previous studies have shown that triptolide inhibits the proliferation of breast cancer cells in vitro and more potently reduces growth of estrogen receptor α (ERα)‐positive breast cancer cells than ERα‐negative cells. In this study, its ability to block the proliferation of breast cancer and its molecular mechanism of action were investigated. Methods: Cell viability was assessed by PrestoBlue assay. Real‐time PCR and western were used to determine ERα expression. To further investigate the effect of ERα on triptolide inhibition of cell growth, MDA‐MB‐231 cells that overexpress ERα were used. The MCF‐7 xenograft mouse tumor model was used to measure the effects of triptolide on breast cancer in vivo. Results: Levels of ERα and phosphorylated ERK were reduced by triptolide. Overexpression of ERα in MDA‐MB‐231 cells significantly enhanced triptolide’s inhibitory effects. In vivo tumor xenograft model, treatment of triptolide significantly reduced tumor size and ERα expression and inhibited phosphorylated ERK expression. Conclusions: This result suggests that triptolide might be a candidate for prevention of ER‐positive breast cancer cell lines.