Two miRNAs (miR-34a, miR-221) were significantly up-regulated and five miRNAs (miR-16, miR-23-3p, miR-122-5p, miR-198, miR-199a-3p) were significantly down-regulated in HCC compared to LC patients.
We sought to develop inorganic-organic hybrid vehicle for the systemic delivery of the tumor suppressor miR-34a, and to investigate the efficiency of the delivered miR-34a in the treatment of HCC in vitro and in vivo.
CA9 expression levels were also correlated with miR-34a levels and rs1048638 genotypes in HCC patients. rs1048638 influences HCC risk and progression through effects on miR-34a-targeted CA9 expression in HCC.
Here, we describe a hepatocellular carcinoma (HCC) cell-based luciferase reporter system which could be used to screen for small molecule modulators of tumor suppressor microRNA-34a.
Previous studies have focused on the association of miR-34 family members with carcinogenesis of many cancers, including hepatocellular carcinoma (HCC).
Numerous studies have focused on the association between miR-34 family members, which are direct p53 targets, and carcinogenesis of many cancers, including hepatocellular carcinoma (HCC).
In contrast, there was a negative correlation between levels of microRNA 34a and lincRNA-UFC1 in HCC tissues; microRNA 34a reduced the stability of lincRNA-UFC1.
Here, we found that the expression of microRNA-34a-5p (miR-34a-5p) was significantly decreased in patients with hepatitis B virus (HBV)-activated liver fibrosis and HCC, as well as in CC14 (Carbon tetrachloride Tetrachloromethane) induced liver fibrosis model mice.
Moreover, in vitro and in vivo studies showed that exo-circ-DB promotes HCC growth and reduces DNA damage via the suppression of miR-34a and the activation of deubiquitination-related USP7.
Since miR-122 and miR-34a downregulation is a common feature in spontaneous human hepatocarcinoma, our finding that these miRNAs are able to target FUT8 3'UTR suggests that, together with transcriptional and other post-transcriptional systems, a miRNA-mediated mechanism could also be involved in the increased core fucosylation observed in liver tumors.
In the present study, the expression of miR‑34a in human liver cancer tissues and cell lines was evaluated and the effects of miR‑34a on cell proliferation, invasion and glycolysis in hepatocellular carcinoma (HCC) cells were determined.
Finally, we introduce methods to study TGF-β-regulated miRNAs and their functions in tumor progression and metastasis using an example of publication from our lab demonstrating the presence of a TGF-β-miR-34a-CCL22 signaling axis, which serves as a potent etiological pathway for the development of hepatocellular carcinoma venous metastases.
Therefore, the results of the present study may improve understanding regarding the role of miR-34a in regulating cell proliferation and contribute to the development of novel therapy of HCC.
In this study, we investigated the methylation status of miR-34 family in HCC tumor and adjacent non-tumor tissues using methylation-specific PCR (MSP).
This study aimed to investigate the relationship of a functional variant (rs1057317) at microRNA-34a (miR-34a) binding site in toll-like receptor 4 gene and the risk of hepatocellular carcinoma.
To confirm effect of miR-34a-5p on tumor growth and its possible effect on MCM2, miR-34a-5p mimic and inhibitor was transfected into HCC cell lines (HepG2).