MicroRNA-106 affects the biological behavior of endometrial cancer RL95-2 cells by regulating the PTEN/PI3K/AKT signaling pathway

  Objective  To investigate the effects of microRNA-106 (miR-106) on the proliferation, apoptosis, invasion and migration of endometrial cancer cells (RL95-2 cells) by regulating PTEN/PI3K/AKT signaling pathway.

  Methods  Real-time fluorescent quantitative polymerase chain reaction (qRT-PCR) was used to detect the expression of miR-106 in specimens of endometrial cancer tissues and adjacent tissues. Endometrial cancer RL95-2 cells were cultured in vitro, and were respectively transfected with plasmid inhibiting miR-106 expression (miR-106 inhibitor) and its negative control (NC inhibitor), overexpression plasmid of PTEN (PTEN) and its negative control (pcDNA), overexpression plasmid of PTEN and miR-106 (miR-106 mimics) and its negative control (miR-NC), which were named as miR-106 inhibitor group, NC inhibitor group, PTEN group, pcDNA group, PTEN+miR-106 group and PTEN+miR-NC group in proper sequence, and the control group was set up without transfection. The cell counting kit 8 (CCK-8) method, transwell chamber, and flow cytometry were used to detect the proliferation, invasion and migration, and apoptosis of RL95-2 cells; western blotting (WB) was used to detect the expression of PTEN/PI3K/AKT pathway related proteins in RL95-2 cells. Dual luciferase reporter gene experiment was used to verify the targeting relationship between miR-106 and PTEN.

  Results  The expression of miR-106 in endometrial cancer tissues was significantly higher than that in adjacent tissues (P < 0.05); the dual luciferase reporter gene experiment confirmed that miR-106 had a targeting relationship with PTEN. After inhibition of miR-106 expression or overexpression of PTEN, the proliferation ability, cell migration and invasion numbers of the RL95-2 cells as well as expression levels of p-PI3K and p-AKT proteins were significantly reduced, while the apoptosis rate was significantly increased (P < 0.05); overexpression of miR-106 could significantly reverse the inhibitory effects of overexpression of PTEN on the proliferation, migration and invasion of RL95-2 cells and the promotion effect on apoptosis (P < 0.05).

  Conclusion  MiR-106 can target and inhibit the expression of PTEN and promote the proliferation, migration and invasion of human endometrial cancer cells by activating the PI3K/AKT pathway, and inhibit cell apoptosis.