MiR-23b functions as an oncogenic miRNA by downregulating Mcl-1S in lung cancer cell line A549.

It has been reported that microRNA-23b (miR-23b) plays a role in multiple cancers, while its impact on lung cancer has not been comprehensively known. Our study explored the probable impacts of miR-23b on lung cancer cells. Expression of miR-23b was assessed by reverse transcription quantitative polymerase chain reaction. After miR-23b mimic, inhibitor, and their own control were transfected into A549 cells, cell viability, migration, invasion, apoptosis, and epithelial-mesenchymal transition (EMT) were investigated through different experimental methods. The targeting contact between miR-23b and myeloid cell leukemia-1 (Mcl-1) was investigated applying dual-luciferase activity assay. In addition, the modulatory impacts of miR-23b on the splicing variants of Mcl-1 (Mcl-1S and Mcl-1L) were explored. MiR-23b was highly expressed in lung cancer cells compared with normal lung cells. Increased expression of miR-23b promoted A549 cell viability, migration, invasion, and EMT. However, miR-23b silencing produced the opposite results. Mcl-1 has been proven to be a specialized target of miR-23b. Compared with the reduction of Mcl-1S induced by miR-23b overexpression, Mcl-1L showed negligible interaction with miR-23b. Moreover, the antitumor activities of miR-23b silencing were alleviated by Mcl-1S silencing. The blockage of Janus kinase/signal transducer and activator of transcription protein (JAK/STAT) and Wnt/ß-catenin induced by miR-23b silencing was reversed by Mcl-1S silencing. MiR-23b might be an up-and-coming biomarker of lung cancer. In addition, miR-23b was involved in the tumor-promoting effects and the mobilization of JAK/STAT and Wnt/ß-catenin pathways through the reduction of Mcl-1S.