Effects of cisplatin on the proliferation, invasion and apoptosis of breast cancer cells following β‑catenin silencing.

Resistance to the chemotherapeutic drug cisplatin has been documented in various types of cancer, while the increased expression of betacatenin has been observed in cisplatinresistant ovarian cancer. However, the involvement of betacatenin in cisplatin resistance is unclear. The present study investigated the antitumor effect of cisplatin on the proliferation, invasion and apoptosis of breast cancer (BC) cells following betacatenin silencing in BC, which is the most frequent type of malignancy among women. The expression of betacatenin in BC tissues and cell lines was measured by reverse transcriptionquantitative polymerase chain reaction, and the association between expression levels and clinical characteristics was statistically analyzed. The viability of BC cell lines treated with siRbetacatenin or with siRbetacatenin and cisplatin in combination was determined using a Cell Counting Kit8 assay. The migratory and invasive abilities of BC cells treated with both siRbetacatenin and cisplatin were examined with Transwell assays. The CD44 antigen/intercellular adhesion molecule 1 expression ratio, cell cycle distribution and apoptosis levels of BC cells treated with siRbetacatenin and cisplatin in combination were detected by flow cytometry. The expression levels of apoptosisassociated proteins, including caspase3/9, in the BC cells treated with both siRbetacatenin and cisplatin were investigated by western blot analysis. The levels of apoptosis in the BC cells following combined treatment with siRbetacatenin and cisplatin was further quantified by Hoechst 33342 staining. betacatenin was identified to be highly expressed in BC tissues and cell lines and was associated with pathological stage and lymph node status. Following knockdown of betacatenin expression, cisplatin treatment suppressed the viabilities, and the migratory and invasive capabilities of the T47D and MCF7 cells, and induced extensive apoptosis. betacatenin knockdown upregulated caspase3/9 levels following cisplatin treatment and induced the apoptosis of T47D and MCF7 cells. In conclusion, betacatenin may be of value as a therapeutic target during cisplatin treatment in patients with BC treated with cisplatin.