KRAS gene silencing inhibits the activation of PI3K-Akt-mTOR signaling pathway to regulate breast cancer cell epithelial-mesenchymal transition, proliferation and apoptosis

OBJECTIVE Our study was performed to investigate the effect of KRAS gene silencing on epithelial-mesenchymal transition (EMT), proliferation, and apoptosis of breast cancer cells by mediating PI3K-Akt-mTOR signaling pathway. MATERIALS AND METHODS The positive rate of KRAS protein expression was detected in tissues collected from breast cancer patients, associated with the analysis of the relationship between KRAS protein expression and clinicopathological features of patients. The expression of KRAS in breast cancer cell lines was tested to screen the suitable cell line. After cell transfection and grouping, qRT-PCR and Western blot were then used to detect the mRNA and protein expression in each group. MTT assay and flow cytometry detected cell proliferation, cell cycle, and apoptosis, respectively. RESULTS The expression of KRAS in cancer tissue was much higher than that in paracancerous normal tissue, and its high expression was correlated statistically with lymph node metastasis, distant metastasis, and tumor infiltration level of patients (all p 0.05). CONCLUSIONS Silencing of KRAS gene expression may inhibit the activation of PI3K-Akt-mTOR signaling pathway, and thus inhibit EMT, proliferation and apoptosis of breast cancer cells. By contrast, activation of the studied signaling pathway can reverse the positive effect of KRAS gene silencing.