miR-203 is an epigenetically silenced tumor-suppressive microRNA in tumors. This study was designed to investigate the effects of miR-203 on the proliferation, migration, invasion, and apoptosis of bladder cancer (BCa) cells. The expression levels of miR-203 in BCa tissues, normal adjacent tissues, and BCa cell lines were detected. BCa cells were transfected with miR-203 mimic and inhibitor to investigate the effect of miR-203 on cell functions and the epithelial-mesenchymal transition (EMT). Cotransfection with miR-203 inhibitor and shRNA of the predicted target gene Twist1 (si-Twist1) was performed to investigate the target relationship of miR-203 and Twist1. The effects of knockdown of Twist1 on cell functions were also investigated. The expression of miR-203 was significantly reduced in BCa tissues and cells, in comparison with the control. miR-203 mimic significantly reduced cell viability, invasion, migration, and EMT, and enhanced cell apoptosis. On the contrary, miR-203 inhibitor showed the opposite results. However, the administration of si-Twist1 cancelled the effect of miR-203 inhibitor on cell proliferation, apoptosis, invasion, and migration. These demonstrated that miR-203 may function as a tumor-suppressive microRNA in BCa by negatively targeting Twist1. Both Twist1 and miR-203 might be explored as potential targets for studying the mechanism related to BCa pathogenesis and therapy.

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Locoregional lymph nodes metastasis in oral tongue squamous cell carcinoma represents one of important and common prognostic factors for poor clinical outcome. The human Telomerase Reverse Transcriptase (hTERT) is one of key players in cancer metastasis and stemness, but its exact function in tongue squamous cell carcinoma remains unknown. Here, we aim to understand the role of hTERT by utilizing the CRISPR/Cas9 gene editing system to deplete hTERT in the SCC-15 cell line. Functional comparison of SCC-15 control and knockout cells (hTERT−/−) showed that loss of hTERT suppressed cell proliferation and migration/invasion. Furthermore, hTERT depletion significantly decreased tumorigenesis, including alterations in cellular morphology that areindicative for epithelial-mesenchymal transition (EMT). Mechanistically we demonstrated that the hTERT knockout attenuates NF-κB signaling via a negative feedback regulation in tumorprogression. From these results we propose a novel molecular mechanism of hTERT to promote SCC-15 invasion and metastasis via NF-κB activation. We conclude that targeting hTERT may represent a new therapeutic strategy to improve therapy and survival of tongue squamous cell carcinoma patients.