Abstract
MicroRNAs (miRNAs) are short, non-coding and endogenous RNAs that played as important roles in the proliferation and metastasis of tumors. In this study, we determined the role of miR-18a in the regulation of HCC cell motility. We showed that miR-18a expression was upregulated in human HCC tissues and cell lines. Moreover, Elevated expression of miR-18a promoted the HCC cell proliferation and migration. KLF4 was identified as a direct target of miR-18a in HCC cells. Furthermore, overexpression of KLF4 attenuated the effects of miR-18a on the regulation of HCC cell motility. The expression of KLF4 was negatively associated with the expression of miR-18a expression in HCC tissues. We also showed that the cell cycle inhibitor p21 was aberrantly downregulated in HCC cells, whereas this inhibition was reversed by miR-18a inhibitor. These data indicated that miR-18a may play a positive role in hepatocellular carcinoma by promoting the proliferation and migration of HCC cells through targeting KLF4 as well as downstream p21.
Highlights
Hepatocellular carcinoma (HCC) is one of the most frequent and most lethal types of cancer worldwide with hardly any effective treatment available far [1, 2]
We showed that miR-18a expression was upregulated in human HCC tissues and cell lines
We found that Krüppel-like factor 4 (KLF4) is a potential direct target of miR-18a with a binding site in the 3’-UTR and investigated the role of miR-18a in regulating hepatocellular carcinoma cell proliferation and migration. miR-18a was found to be significantly upregulated in HCC and promotes hepatocellular carcinoma cell motility by inhibiting KLF4
Summary
Hepatocellular carcinoma (HCC) is one of the most frequent and most lethal types of cancer worldwide with hardly any effective treatment available far [1, 2]. Early detection, surgical resection and gene therapy are the major treatment approaches for HCC [3]. Despite significant improvements in diagnostic method and surgical therapy, the cure rate of HCC is very low. Knowledge about the molecular mechanisms underlying HCC progression is an urgent need to improve the understanding of, and therapeutic strategies for, human HCC. Ectopic regulation of miRNA expression has been reported widely and proven to be associated with cancer progression in glioma, metastatic prostate cancer, hepatocellular carcinoma, and others [8, 9]. Various studies reported the differential expression of miRNAs in patients with hepatocellular carcinoma, including miR-135a, miR-33a, miR-320a, miR-122, and miR-31 [10,11,12,13,14]
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