Taken together, these findings indicated that LINC00511 interacted with EYA1 promoted HCC development via mediating miR-195, proposing a promising therapeutic biomarker for HCC diagnosis and prognosis.
The expression levels of miR-195 were detected in 120 HCC patients, 64 hepatitis only patients, and 118 healthy control as well as 4 HCC cell lines, by using quantitative real-time PCR.
These results indicated that SNHG1 participated in the development of hepatocellular carcinoma as a ceRNA to competitively bind to miR-195-5p and thus mediate PDCD4 expression.
In vitro, loss-of-function experiments revealed that SNHG16 knockdown suppressed the proliferation and weakened invasion of SMMC7721 and HepG2 cells. miR-195 expression was significantly decreased in HCC tissues and negatively correlated with SNHG16 expression.
Malat1 silence could not suppress HCC cell growth and motility when miR-195 was knocked down.EGFR was a direct target of miR-195. miR-195 overexpression could not suppress HCC cell growth and motility when the 3'UTR site of EGFR was overexpressed.
Lastly, we revealed YAP was not only the downstream of miR-195 in HCC, but also mediated the promoting effects of miR-195 on the metastasis and EMT of HCC cells.
In the present study, the expression of miR-195 was determined to be markedly downregulated in HCC tissues and cell lines, as compared with normal liver cells.
Consistently, substantial increase of HDAC3 protein was detected in human HCC tissues and HDAC3 upregulation was significantly correlated with miR-195 downregulation, suggesting that HDAC3 elevation may represent an important cause for miR-195 reduction in HCC.
Further, the serum levels of exosomal miR-101, miR-106b, miR-122 and miR-195 were lower in patients with HCC than in patients with CHB (P=0.014, P<0.001, P<0.001 and P<0.001, respectively).
Five of them (miR-148a, miR-375, miR-195, miR-497 and miR-378) were in hypermethylation and down-regulation status, while another five (miR-106b, miR-25, miR-93, miR-23a and miR-27a) were in hypomethylation and up-regulation status in HCC.
Taken together, our results suggest that miR-195, a tumor suppressor miRNA, contributes to the lung metastasis of HCC by negatively regulating FGF2 and VEGFA, providing key implications of miR-195 for the therapeutic intervention of HCC.
The miR-195 expression levels were found to be reduced in HCC tissues and cell lines. miR-195 overexpression resulted in a reduction in cell proliferation.
In the current study, by way of informatics software, we found that MicroRNA-195 (miR-195) could negatively regulate protein levels of SRC-3 through targeting its 3'-untranslated region (3'-UTR) in hepatocellular carcinoma (HCC) cells.
Moreover, target genes frequently upregulated in HCC in a tumor-specific manner, such as CDK6, CCNE1, CDC25A and CDK4, showed an inverse correlation in the expression of miR-195 and miR-497, and their targets.
These results indicate that miR-195 could improve the drug sensitivity at least in part by targeting Bcl-w to increase cell apoptosis in hepatocellular carcinoma cells.
We investigated whether measurement of serum levels of the microRNAs (miRNAs) miR-16, miR-195, and miR-199a, alone or in combination with conventional serum markers, can help to differentiate hepatocellular carcinoma (HCC) from chronic liver diseases (CLDs).