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miR-429 represses cell proliferation and induces apoptosis in HBV-related HCC
1Jining Medical University, Jining 272067, PR China.
Abstract:
MicroRNAs are a class of endogenous non-coding RNAs that regulate gene expression at post-transcriptional level, thus participating in diverse biological pathways. Increasing miRNAs are found to dysregulate hepatocellular carcinoma (HCC) and are involved in liver tumorigenesis. In this study, miR-429 was found to obviously downregulate much more in hepatitis B virus (HBV)-related hepatocellular carcinoma. To evaluate the effects of miR-429, miR-429 was over-expressed in HepG2.2.15 cells. The results have proved that overexpression of miR-429 decreased cell proliferation and induced cell apoptosis. Further, overexpression of miR-429 can suppress the secretion of HBsAg and HBeAg. In concordance to this, the level of NOTCH1 expression was high in human HBV-related HCC tissues and HepG2.2.15 cells. MiR-429 directly targeted NOTCH1 and reduced both mRNA and protein levels of NOTCH1 which stimulated proliferation and suppressed apoptosis in HCC cells. Our results provide new insight into the function of miR-429 in HBV-related HCC. It is beneficial to insight into the mechanism of HBV infection and pathophysiology of HBV-related HCC.
Insights
MicroRNA-429 is downregulated in hepatitis B virus-related liver cancer. Restoring miR-429 levels inhibits cancer cell growth and promotes apoptosis by targeting NOTCH1, offering new insights into hepatocellular carcinoma mechanisms.
Area of Science:
- Molecular Biology
- Oncology
- Virology
Background:
- MicroRNAs (miRNAs) are key regulators of gene expression, crucial in various biological processes.
- Dysregulation of miRNAs is increasingly implicated in the development of hepatocellular carcinoma (HCC).
- Hepatitis B virus (HBV) infection is a major cause of HCC worldwide.
Purpose of the Study:
- To investigate the role of miR-429 in HBV-related HCC.
- To elucidate the molecular mechanisms underlying miR-429's function in liver tumorigenesis.
Main Methods:
- Overexpression of miR-429 in HepG2.2.15 cells (an HBV-producing cell line).
- Assessment of cell proliferation, apoptosis, and secretion of HBV antigens (HBsAg, HBeAg).
- Analysis of NOTCH1 expression at mRNA and protein levels in HCC tissues and cell lines.
Main Results:
- miR-429 was significantly downregulated in HBV-related HCC tissues.
- Overexpression of miR-429 reduced cell proliferation and induced apoptosis in HepG2.2.15 cells.
- miR-429 suppressed HBsAg and HBeAg secretion and directly targeted NOTCH1, decreasing its expression.
Conclusions:
- miR-429 plays a tumor-suppressive role in HBV-related HCC.
- The miR-429/NOTCH1 axis is a critical pathway in HBV-associated liver cancer.
- Understanding this mechanism provides novel insights into HBV infection and HCC pathophysiology.
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