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MicroRNAs have emerged as crucial regulators of tumorigenesis. However, the mechanism by which miR‑203 is involved in the pathogenesis of pancreatic cancer (PC) remains elusive. In the present study, PC cell lines were used as an experimental model to investigate the expression and functional role of miR‑203 in PC. miR‑203 mimic virus, miRNA negative control virus and Survivin shRNA virus were transfected into the PC cell line, CFPAC‑1. mRNA and protein levels of Survivin were detected using qPCR and western blot analysis. Proliferation, apoptosis and cell cycle profiles were detected by an MTT assay and flow cytometry. Female BALB/cA‑nu nude mice were used to validate the role of miR‑203 in vivo. The protein levels of Survivin were found to negatively correlate with miR‑203 levels in four PC cell lines. A luciferase assay revealed that Survivin was a direct target of miR‑203. Transfection with miR‑203 mimic inhibited CFPAC‑1 cell proliferation and induced apoptosis and G1 phase cell cycle arrest, similar to knockdown of Survivin. In the in vivo nude mouse model, the downregulation of Survivin by knockdown of Survivin or transfection with miR‑203 mimic inhibited tumor growth. Results of the current study indicate that miR‑203 regulates the proliferation, apoptosis and cell cycle progression of PC cells by targeting Survivin.

miR-203 regulates the proliferation, apoptosis and cell cycle progression of pancreatic cancer cells by targeting Survivin