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 beta-catenin has been observed in cisplatin-resistant ovarian cancer. However, the involvement of beta-catenin 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 beta-catenin silencing in BC, which is the most frequent type of malignancy among women. The expression of beta-catenin in BC tissues and cell lines was measured by reverse transcription-quantitative polymerase chain reaction, and the association between expression levels and clinical characteristics was statistically analyzed. The viability of BC cell lines treated with siR-beta-catenin or with siR-beta-catenin and cisplatin in combination was determined using a Cell Counting Kit-8 assay. The migratory and invasive abilities of BC cells treated with both siR-beta-catenin 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 siR-beta-catenin and cisplatin in combination were detected by flow cytometry. The expression levels of apoptosis-associated proteins, including caspase-3/9, in the BC cells treated with both siR-beta-catenin and cisplatin were investigated by western blot analysis. The levels of apoptosis in the BC cells following combined treatment with siR-beta-catenin and cisplatin was further quantified by Hoechst 33342 staining. beta-catenin 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 beta-catenin expression, cisplatin treatment suppressed the viabilities, and the migratory and invasive capabilities of the T47D and MCF-7 cells, and induced extensive apoptosis. beta-catenin knockdown upregulated caspase-3/9 levels following cisplatin treatment and induced the apoptosis of T47D and MCF-7 cells. In conclusion, beta-catenin may be of value as a therapeutic target during cisplatin treatment in patients with BC treated with cisplatin.