MiR-520b inhibited metastasis and proliferation of non-small cell lung cancer by targeting CHAF1A.

Abstract

To investigate the potential effect of miR-520b on the development of non-small cell lung cancer and to explore the underlying mechanism. The expression levels of miR-520b in non-small cell lung cancer (NSCLC) tissues and cells (A549), as well as corresponding adjacent normal tissues and normal human lung epithelial cells (BEAS-2B), were detected by quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR), respectively. Luciferase reported gene assay was performed to evaluate the interaction between miR-520b and chromatin assembly factor 1 subunit A (CHAF1A). Meanwhile, the effect of the miR-520b/CHAF1A axis on A549 cells was determined by subsequent experiments, including CHAF1A expression detection, cell proliferation, migration and invasion. MiR-520b was lowly expressed in NSCLC tissues than that of corresponding adjacent normal tissues. Same results were obtained at the cellular level. To investigate the potential targets of miR-520b, we searched three publicly available algorithms, including TargetScan, miRDB and microRNA. Results indicated that CHAF1A was a direct target of miR-520b. Meanwhile, the luciferase reporter gene assay confirmed our hypothesis. Subsequent experiments demonstrated that decreased expression of CHAF1A resulting from the up-regulation of miR-520b could decelerate the proliferation, invasion and migration of lung cancer cells. We discovered the inhibitory function of miR-520b in NSCLC by targeting CHAF1A. Moreover, our study revealed that the miR-520b/CHAF1A axis might be a potential therapeutic target for the treatment of NSCLC.