Phosphatase and tensin homolog regulates microRNA-182 and AKT to induce apoptosis of breast cancer cells SKBR3

Breast cancer is a disease of high incidence impacting the health of numerous female patients. Phosphatase and tensin homolog (PTEN) is involved in breast cancer cell apoptosis, however, the underlying mechanism is largely unknown. This study aims to explore the role and mechanism of PTEN in breast cancer cell apoptosis. Breast cancer cells SKBR3 were transfected with the overexpression vector of PTEN, and then cell apoptosis was assessed by flow cytometry. The phosphorylated level of v-akt murine thymoma viral oncogene homologs (p-AKT) and the level of microRNA-182 (miR-182) were detected in order to analyze the mechanism of PTEN in regulating SKBR3 cell apoptosis. Besides, miR-182 mimic was transfected to detect changes in apoptosis and AKT activation. Results showed that PTEN overexpression suppressed p-AKT level and induced SKBR3 cell apoptosis (P < 0.01). It also down-regulated miR-182 and miR-183 levels (P < 0.001), but did not affect miR-96 level (P > 0.05). miR-182 mimic promoted p-AKT and suppressed cell apoptosis (P < 0.05), which attenuated the effects of PTEN overexpression, implying the involvement of miR-182 in the mechanism of PTEN functions. These findings provide fundamental evidence for the potential application of PTEN in molecular therapy for breast cancer. The mechanism of PTEN in regulating breast cancer cell apoptosis may be related to its suppression on miR-182 and AKT activation. Further research will be necessary to take full advantage of PTEN in managing breast cancer.