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

Abstract

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/β‐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/β‐catenin pathways through the reduction of Mcl‐1S.

Hsa_circ_0021727 (circ-CD44) promotes ESCC progression by targeting miR-23b-5p to activate the TAB1/NFκB pathway

“…In addition, miR-23b was identified to act both as an oncogene and as a tumor suppressor. Increased expression of miR-23b promoted lung cancer cells viability, migration, invasion, and EMT [ 56 ]. miR-23b inhibits cell migration and invasion through targeting phosphodiesterase 7A (PDE7A) in colon cancer cells [ 57 ].…”

Lnc-PLA2G4A-4 facilitates the progression of hepatocellular carcinoma by inducing versican expression via sponging miR-23b-3p

“…In our research, we identified some possible binding microRNAs of Lnc-PLA2G4A-4 by bioinformatic prediction, which were reported to regulate tumor progression, such as miR-23b, miR-567 and miR-888. Among them, miR-23b-3p attracted our attention, because it acts as both a tumor suppressor [ [35] , [36] , [37] ] and an oncogenic miRNA [ [38] , [39] , [40] ] in various types of carcinogenesis. There is accumulating evidence that miR-23b performed a variety of functions in various tumor progressions, which is involved in proliferation [ 41 ], apoptosis [ 42 ], metastasis [ 43 ], angiogenesis [ 44 ], chemoresistance [ 45 ] and glycolysis [ 45 ].…”

MicroRNA‑182 promotes epithelial‑mesenchymal transition by targeting FOXN3 in gallbladder cancer

“…miR-425 has been demonstrated to promote cell proliferation, migration, invasion and EMT by activating the β-catenin pathway (29). miR-23b is involved in tumor-promoting effects, which are associated with the activation of the JAK/STAT and Wnt/β-catenin pathways in A549 cells (30). In addition, the key EMT factor, ZEB1, is transcriptionally regulated by the β-catenin/TCF4 complex (11).…”