MicroRNA-641 inhibits lung cancer cells proliferation, metastasis but promotes apoptosis in cells by targeting PDCD4.

Dysregulation of microRNAs (miRNAs) are found in various human cancers, but the roles of miR-641 in lung cancer are still unclear. Our purpose is to explore miR-641 effects on the cellular behavior of A549 cells and the related molecular mechanisms. RT-qPCR assay was conducted to examine the expression of miR-641 in lung cancer and normal lung cell lines. A549 cells were transfected with miR-641 mimic and inhibitor, programmed cell death 4 (PDCD4) targeted siRNA and corresponding controls. Then, cell viability, migration, invasion and apoptosis were analyzed by Cell Counting Kit-8 (CCK-8), Transwell and flow cytometry assays. The expression of apoptosis-related factors and epithelial mesenchymal transition (EMT)-related factors were detected by western blot and RT-qPCR. A target gene of miR-641 was validated by dual-luciferase assay. Besides, the main factors expressions of JAK/STAT and PI3K/AKT signal pathways were measured by western blot. Results showed that miR-641 was low expressed in A549, H1650 and H1299 cells compared to WI-38 and HEL-1 cells. MiR-641 overexpression inhibited cell viability, migration, invasion but promoted apoptosis and apoptosis-related factors levels. Moreover, miR-641 overexpression inhibited TGF-β1-induced EMT in A549 cells. Additionally, PDCD4 was a direct target of miR-641 and PDCD4 silencing notably induced apoptosis, and relieved miR-641 suppressing promoted cell viability, migration and invasion. Finally, PDCD4 silencing blocked miR-641 suppression-induced activations of JAK/STAT and PI3K/AKT signal pathways. In conclusion, miR-641 inhibited cell proliferation and metastasis but promoted apoptosis in lung cancer cells by targeting PDCD4 and blocking JAK/STAT and PI3K/AKT signal pathways.