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Updated: May 3, 2026
Efficient Gene Knockdown in the Liver via Intrasplenic Injection of Adeno-Associated Virus Serotype 8 (AAV8)-Delivered Small Hairpin RNA
Published on: November 1, 2024
Recombinant adenovirus encoding FAT10 small interfering RNA inhibits HCC growth in vitro and in vivo
Jingxiang Chen1, Li Yang2, Hongxu Chen1
1Department of Hepatobiliary Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042, China.
Abstract:
Hepatocellular carcinoma is an aggressive and rapidly fatal malignancy representing the common cancer worldwide. The specific cellular gene involved in carcinogenesis has not been fully characterized. The ubiquitin-like modifier FAT10, recently reported to be overexpressed in 90% of hepatocellular carcinoma carcinomas, was attributed to transcriptional upregulation upon the loss of p53 and induced chromosome instability in long-term in vitro culture. However, the exact function of FAT10 in hepatocellular carcinoma is not clear. In the present study, we utilized adenovirus-mediated RNA interference to knock down FAT10 expression in hepatocellular carcinoma cells and observed its effects on hepatocellular carcinoma cell growth in vitro and in vivo. The results demonstrated that interference of FAT10 could inhibit cell proliferation by inhibiting the cell cycle S-phase entry and inducing cell apoptosis. In addition, in vivo experiments showed that adenovirus Ad-siRNA/FAT10 significantly suppressed tumor growth and prolonged the lifespan of tumor-bearing mice. These results suggest that knockdown of FAT10 by adenovirus-delivered siRNA may be a promising therapeutical strategy for treatment of hepatocellular carcinoma.
Insights
Knocking down FAT10, a gene overexpressed in liver cancer, inhibits cancer cell growth and induces apoptosis. This approach shows promise for treating hepatocellular carcinoma in mice.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Hepatocellular carcinoma (HCC) is a prevalent and aggressive cancer with poorly understood genetic drivers.
- The ubiquitin-like modifier FAT10 is overexpressed in most HCC cases, linked to p53 loss and chromosomal instability.
- The precise role of FAT10 in HCC development and progression remains unclear.
Purpose of the Study:
- To investigate the functional role of FAT10 in hepatocellular carcinoma.
- To evaluate the therapeutic potential of targeting FAT10 in HCC.
Main Methods:
- Adenovirus-mediated RNA interference (siRNA) was used to reduce FAT10 expression in HCC cells.
- In vitro assays assessed the impact on cell proliferation, cell cycle progression, and apoptosis.
- In vivo studies in tumor-bearing mice evaluated the effect on tumor growth and survival.
Main Results:
- Interference with FAT10 expression significantly inhibited HCC cell proliferation.
- FAT10 knockdown led to cell cycle arrest at the S-phase and induced apoptosis.
- Adenovirus-delivered siRNA targeting FAT10 suppressed tumor growth and extended lifespan in mice.
Conclusions:
- FAT10 plays a crucial role in promoting HCC cell growth and survival.
- Targeting FAT10 via adenovirus-mediated siRNA represents a potential therapeutic strategy for hepatocellular carcinoma.
- Further research into FAT10-targeted therapies could offer new treatment options for HCC patients.
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