Downregulation of KIF21B by miR-132-3p suppresses cellular functions in gastric cancer via regulating Wnt/β-catenin signaling pathway

Abstract Recently, kinesin family member 21B (KIF21B) has been reported to be an oncogene in non-small cell lung cancer and hepatocellular carcinoma. However, the functional role and related mechanisms underlying gastric cancer (GC) pathogenesis remain largely uncovered. Here, we first found that the expression of KIF21B was upregulated in GC tissues compared with adjunct normal tissues by analysis of Oncomine microarray gene expression datasets and clinical specimens. Knockdown of KIF21B significantly suppressed the proliferation, migration and invasion in GC cell lines using CCK-8 assay and transwell assay. By luciferase reporter assay, KIF21B was confirmed as the target of miR-132-3p in GC cells and suppressed after miR-132-3p overexpression. Moreover, miR-132-3p was down-regulated and inversely correlated with KIF21B expression in GC tissues. Further functional experiments demonstrated that overexpression of KIF21B remarkedly reversed the suppressive effects of miR-132-3p overexpression on GC cell proliferation, migration and invasion. Furthermore, western blot analysis manifested that miR-132-3p overexpression downregulated the protein levels of Wnt1, c-Myc, β-catenin, PCNA and N-cadherin, and upregulated E-cadherin expression in GC cells, which were all alleviated after KIF21B overexpression. In summary, our findings provide the first evidence that down-regulation of KIF21B by miR-132-3p suppresses cellular functions in gastric cancer via regulating Wnt/β-catenin signaling.