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

Jianhong Zhang, Zeming Hu, Chao Wen, Qicheng Liao, Baoqing He, Jing Peng, Xin Tang, Zhixi Chen, Yuankang Xie

2021Oncology Letters17 citationsDOIOpen Access PDF

Abstract

Increasing evidence has suggested an association between the expression profiles of microRNAs (miRs) and gallbladder cancer (GBC). Recently, miR-182 has been demonstrated to exert tumor-promoting effects. However, the biological activity and molecular mechanisms of miR-182 in GBC remain unclear. The results of the present study demonstrated that miR-182 expression was significantly upregulated in GBC tissues and cell lines (GBC-SD and SGC-996). In addition, miR-182-knockdown attenuated epithelial-mesenchymal transition (EMT) in GBC cells, as indicated by decreased cell migratory and invasive abilities, decreased vimentin expression, and increased E-cadherin expression. The activities of β-catenin and its downstream factors, Cyclin D1 and c-Myc, were also demonstrated to decrease following miR-182-knockdown. Forkhead box N3 (FOXN3) was identified as the direct target of miR-182. Overexpression of FOXN3 ameliorated EMT and the β-catenin pathway. Taken together, the results of the present study suggested that miR-182 promotes EMT in GBC cells by targeting FOXN3, which suppresses the Wnt/β-catenin pathway.

Topics & Concepts

Epithelial–mesenchymal transitionGene knockdownOncogeneVimentinCyclin D1Wnt signaling pathwayCancer researchmicroRNACell cycleGallbladder cancerCancerDownregulation and upregulationBiologyMolecular medicineApoptosisCell biologyMetastasisSignal transductionImmunohistochemistryImmunologyGeneBiochemistryGeneticsMicroRNA in disease regulationCircular RNAs in diseasesCancer-related molecular mechanisms research