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MicroRNA-452 promotes tumorigenesis in hepatocellular carcinoma by targeting cyclin-dependent kinase inhibitor 1B

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Abstract

Dysregulation of miR-452 has been observed in many tumors, but its biological function in hepatocellular carcinoma (HCC) is still unknown. Our results showed that miR-452 expression is significantly increased in HCC tissues and HCC cell lines. We also found that overexpression of miR-452 dramatically accelerated proliferation, induced cell cycle from G1 to S transition, and blocked apoptosis of HCC cells. Migration and matrigel invasion assays indicated that miR-452 significantly promotes HepG2 and QGY-7703 cells migration and invasion in vitro. Further studies showed that miR-452 directly targets the 3′-untranslated region of cyclin-dependent kinase inhibitor 1B (CDKN1B), ectopic miR-452 expression suppressed CDKN1B expression on mRNA and protein level. Silencing CDKN1B by small interfering RNA resembled the phenotype resulting from ectopic miR-452 expression. This study provides new insights into the potential molecular mechanisms that miRNA-452 contributed to HCC.

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Acknowledgments

This work was supported by grants from National Natural Science Foundation of China (Nos. 31300718 and 31200974), Zhejiang Natural Science Foundation (No. Y204499), and Universities of Zhejiang the most important Biology Subject (a) Foundation.

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Correspondence to Yaozhou Zhang.

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Zheng, Q., Sheng, Q., Jiang, C. et al. MicroRNA-452 promotes tumorigenesis in hepatocellular carcinoma by targeting cyclin-dependent kinase inhibitor 1B. Mol Cell Biochem 389, 187–195 (2014). https://doi.org/10.1007/s11010-013-1940-z

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  • DOI: https://doi.org/10.1007/s11010-013-1940-z

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