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Oncolytic Virus Senecavirus A Inhibits Hepatocellular Carcinoma Proliferation and Growth by Inducing Cell Cycle
Tao Gong1,2, Xiao Liu3, Qingyuan Li1,2
1Department of Clinical Medicine, North Sichuan Medical College, Nanchong, Sichuan, China.
Background And Aims:
Hepatocellular carcinoma (HCC) is a highly aggressive tumor with limited treatment options and high mortality. Senecavirus A (SVA) has shown potential in selectively targeting tumors while sparing healthy tissues. This study aimed to investigate the effects of SVA on HCC cells in vitro and in vivo and to elucidate its mechanisms of action.
Methods:
The cell counting kit-8 assay and colony formation assay were conducted to examine cell proliferation. Flow cytometry and nuclear staining were employed to analyze cell cycle distribution and apoptosis occurrence. A subcutaneous tumor xenograft HCC mouse model was created in vivo using HepG2 cells, and Ki67 expression in the tumor tissues was assessed. The terminal deoxynucleotidyl transferase dUTP nick end labeling assay and hematoxylin and eosin staining were employed to evaluate HCC apoptosis and the toxicity of SVA on mouse organs.
Results:
In vitro, SVA effectively suppressed the growth of tumor cells by inducing apoptosis and cell cycle arrest. However, it did not have a notable effect on normal hepatocytes (MIHA cells). In an in vivo setting, SVA effectively suppressed the growth of HCC in a mouse model. SVA treatment resulted in a significant decrease in Ki67 expression and an increase in apoptosis of tumor cells. No notable histopathological alterations were observed in the organs of mice during SVA administration.
Conclusions:
SVA inhibits the growth of HCC cells by inducing cell cycle arrest and apoptosis. It does not cause any noticeable toxicity to vital organs.
Insights
Senecavirus A (SVA) effectively inhibits hepatocellular carcinoma (HCC) growth by inducing apoptosis and cell cycle arrest. This novel cancer therapy shows promise with no observed toxicity in vital organs.
Area of Science:
- Oncology
- Virology
- Molecular Biology
Background:
- Hepatocellular carcinoma (HCC) is an aggressive cancer with poor prognosis.
- Limited effective treatment options exist for HCC.
- Senecavirus A (SVA) demonstrates selective tumor-targeting capabilities.
Purpose of the Study:
- To evaluate the efficacy of Senecavirus A (SVA) against hepatocellular carcinoma (HCC) cells.
- To investigate the mechanisms underlying SVA's anti-HCC effects.
- To assess SVA's safety profile in vivo.
Main Methods:
- Cell proliferation was assessed using cell counting kit-8 and colony formation assays.
- Cell cycle distribution and apoptosis were analyzed via flow cytometry and nuclear staining.
- An HCC xenograft mouse model was used to evaluate SVA's in vivo efficacy and toxicity.
Main Results:
- SVA suppressed HCC cell proliferation and induced apoptosis and cell cycle arrest in vitro.
- SVA significantly inhibited HCC tumor growth in vivo, reducing Ki67 expression and increasing apoptosis.
- SVA treatment showed no significant toxicity in vital organs of treated mice.
Conclusions:
- Senecavirus A effectively inhibits hepatocellular carcinoma growth through apoptosis and cell cycle arrest.
- SVA exhibits a favorable safety profile, with no notable organ toxicity observed.
- SVA represents a potential therapeutic agent for hepatocellular carcinoma.
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