Abstract
Accumulating evidence verified that microRNAs (miRNAs) participate in the development of several cancers. The levels of miR-138-5p and forkhead box c1 (FOXC1) were examined using quantitative Real-time PCR (qRT-PCR). Cell Counting Kit-8 (CCK-8), colony formation, migration, and Transwell invasion assays were conducted to examine the impact of miR-138-5p on hepatocellular carcinoma (HCC) cells. The protein expression of FOXC1 was detected using Western blotting assay. The tumor growth of HCC cell in vivo was analyzed using transplanted tumor model. The expressions of FOXC1 and Ki67 in vivo were assessed using immunohistochemistry (IHC) assay. We testified that miR-138-5p was down-expressed in HCC and the low level of miR-138-5p was related to the poor clinical outcome of patient with HCC. Moreover, miR-138-5p repressed the growth and metastatic phenotypes of HCC cells. Consistent with the results in vitro investigations, we revealed that miR-138-5p served as a suppressive miRNA in the growth of HCC cell in vivo. By using the luciferase assay and immunoblotting, we validated that FOXC1 was a potential downstream gene of miR-138-5p. Finally, our results showed that re-expression of FOXC1 rescued the growth and metastatic-related traits of HCC cell inhibited by miR-138-5p. Altogether, our observations imply that miR-138-5p restrains the aggressive phenotypes of HCC cell via modulating FOXC1.
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