AI Article Synopsis
- Recent research shows that miRNA, specifically miR-3196, is significant in the development of hepatocellular carcinoma (HCC), but its exact role was previously unclear.
- miR-3196 is found to be downregulated in HCC tissues, with lower levels linked to larger tumor size and advanced TNM stages.
- Increasing miR-3196 levels can suppress HCC cell growth and make them less resistant to chemotherapy, with the tumor suppressor p53 enhancing miR-3196 expression and influencing the negative regulation of FOXP4, contributing to reduced tumor growth and increased cell death.
Article Abstract
Increasing evidences demonstrate that miRNAs play an important role in development and progression of hepatocellular carcinoma (HCC). Recent studies indicate that miR-3196 regulates tumorigenesis in breast and lung cancer. However, its role and regulatory mechanism remains unknown in hepatocellular carcinoma. Here, we found that miR-3196 was downregulated in HCC tissues and decreased miR-3196 was correlated with tumor size (=0.0297) and TNM stage (=0.034). Forced miR-3196 suppressed HCC cell growth and chemoresistance and . Further mechanistic studies revealed that the tumor suppressor p53 transcriptionally upregulated miR-3196 expression by binding to its promoter region in HCC cells. Additional, we also found that FOXP4 was a downstream target of miR-3196 and increased miR-3196 inhibited FOXP4 expression which led to HCC growth suppression and cell apoptosis increase. Collectively, our data shed a new role of miR-3196 in HCC and indicates that p53-dependent, miR-3196-medicated FOXP4 pathway inhibits the tumorigenesis of HCC.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6943357 | PMC |
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