Upregulated MicroRNA-141 Suppresses Epithelial-Mesenchymal Transition and Lymph Node Metastasis via HOXC6-Dependent TGF- β Signaling Pathway in Laryngeal Cancer.

This study investigated the roles of microRNA-141 (miR-141), Homeobox C6 (HOXC6), and the transforming growth factor-β (TGF-β) signaling pathway in epithelial-mesenchymal transition (EMT) and lymph node metastasis in laryngeal cancer. Initially, differentially expressed genes related to laryngeal cancer were retrieved, from which HOXC6 was identified. Next, HOXC6 was determined to be a target gene of miR-141. The regulatory relationship of miR-141, HOXC6 and the TGF-β signaling pathway were then explored accordingly. To further investigate the associated underlying mechanism, Hep-2 cells were transfected with miR-141 mimic, miR-141 inhibitor, and HOXC6-siRNA, after which cell viability, migration, invasion, EMT and tumor growth and metastasis were examined. Laryngeal cancer tissues exhibited downregulated miR-141 and upregulated HOXC6. Overexpressed miR-141 was found to downregulate HOXC6 to inactivate the TGF-β signaling pathway. Upregulated miR-141 or silenced HOXC6 was observed to repress EMT, viability, migration and invasion of laryngeal cancer cells, corresponding to reduced expression levels of vimentin, snail, MMP-2, and MMP-9 as well as elevated expression of E-cadherin. Tumor volume and weight and lymph node metastasis were also inhibited by the upregulated miR-141. Taken together, the key observations of the current study demonstrate that upregulated miR-141 decreases HOXC6 expression, thus inactivating the TGF-β signaling pathway, whereby the EMT and lymph no...
Source: Am J Physiol Cell Ph... - Category: Cytology Authors: Tags: Am J Physiol Cell Physiol Source Type: research