MicroRNA-374b accelerates the development of lung cancer through downregulating PTEN expression via activating PI3K/Akt pathway.

OBJECTIVE

To elucidate whether microRNA-374b could participate in the development of lung cancer (LC) through downregulating PTEN (gene of phosphate and tensin homolog deleted on chromosome ten) expression via activating PI3K/Akt pathway.

PATIENTS AND METHODS

Expression levels of microRNA-374b and PTEN in LC tissues and adjacent normal tissues were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Moreover, the expression level of microRNA-374b in LC cell lines was detected as well. The microRNA-374b inhibitor was constructed and transfected to downregulate microRNA-374b expression in A549 and H358 cells. The regulatory effects of microRNA-374b on migratory and proliferative capacities of LC cells were explored by wound healing and cell counting kit-8 (CCK-8) assay, respectively. After co-transfection of microRNA-374b inhibitor and si-PTEN in LC cells, expression levels of PTEN/PI3K/Akt were determined by qRT-PCR and Western blot.

RESULTS

QRT-PCR results showed that microRNA-374b expression was higher, while PTEN expression was lower in LC tissues than adjacent tissues. Identically, microRNA-374b was also highly expressed in LC cell lines. PTEN expression was negatively correlated with microRNA-374b expression in LC. The downregulation of microRNA-374b in A549 and H358 cells inhibited their migratory and proliferative potentials. Subsequently, we verified that microRNA-374b could bind to PTEN through dual-luciferase reporter gene assay. MicroRNA-374b could inhibit PTEN expression and activate the PI3K/Akt pathway. Furthermore, PTEN knockdown enhanced migratory and proliferative abilities of LC cells, which were attenuated by co-transfection of microRNA-374b inhibitor.

CONCLUSIONS

MicroRNA-374b promotes the development of LC by downregulating PTEN expression through activating PI3K/Akt pathway.