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Published on: October 28, 2014
cPDS Promotes Cell Apoptosis by Reducing the Translational Efficiency of BIRC3 mRNA in HCC
Yiheng Liu1, Qingqing Liu1, Tianyi Huang1
1Department of Gastroenterology, Affiliated Hospital of Nantong University, Medical School of Nantong University, Nantong, 226001, China.
Background:
Hepatocellular carcinoma (HCC) is one of the primary liver tumors with high incidence and mortality. RNA G-quadruplexes (rG4) are nucleic acid structures involved in gene expression and genome duplication. rG4 exerts its function by interacting with rG4-binding proteins. The carboxypyridostatin (cPDS), a specific ligand of rG4, are widely studied in numerous tumors. However, the role of cPDS in HCC and its regulatory mechanisms are not yet fully understood. Our study aimed to discuss the regulatory mode of cPDS on Baculoviral IAP Repeat Containing 3 (BIRC3) expression and its impact on proliferation, apoptosis, and other biologic functions in HCC.
Methods:
We conducted colony formation, CCK8, Edu incorporation, scratch healing, and cell spheroid formation assays to analyze the function of cPDS on cell proliferation and migration. Additionally, we explored the role of cPDS in regulating BIRC3 expression by Western blot and qRT-PCR. Furthermore, we evaluated the impact of BIRC3 on cell proliferation and subcutaneous tumor formation in nude mice. Finally, we analyzed the regulatory mechanisms of cPDS on cell apoptosis by Western blot, qRT-PCR, flow cytometry, and Annexin V-FITC staining.
Results:
Our results demonstrated that cPDS inhibited HCC cells proliferation and migration. Moreover, cPDS elevated the mRNA level while inhibiting the protein expression of BIRC3 in HCC cells. Overexpression of BIRC3 significantly enhanced the proliferation of HCC cells. In the nude mice model, BIRC3 significantly increased the tumor volume and weight. Mechanistically, cPDS promoted cell apoptosis via inhibiting BIRC3-mediated anti-apoptotic effect.
Conclusion:
Our findings revealed a critical role of rG4 ligand cPDS in HCC progression and indicate that cPDS may be used for HCC treatment considering its tumor inhibitory properties by regulating cell apoptosis.
Insights
Carboxypyridostatin (cPDS) inhibits hepatocellular carcinoma (HCC) progression by reducing cell proliferation and migration. This RNA G-quadruplex ligand impacts Baculoviral IAP Repeat Containing 3 (BIRC3) expression, promoting apoptosis for potential HCC treatment.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Hepatocellular carcinoma (HCC) is a prevalent liver tumor with high mortality.
- RNA G-quadruplexes (rG4) are crucial in gene regulation, interacting with proteins.
- Carboxypyridostatin (cPDS), an rG4 ligand, shows potential in cancer therapy, but its role in HCC requires elucidation.
Purpose of the Study:
- To investigate the regulatory effects of cPDS on Baculoviral IAP Repeat Containing 3 (BIRC3) expression in HCC.
- To determine the impact of cPDS on HCC cell proliferation, migration, and apoptosis.
- To explore the therapeutic potential of cPDS in HCC treatment.
Main Methods:
- Cell proliferation and migration assays (colony formation, CCK8, Edu, scratch healing, spheroid formation).
- Analysis of BIRC3 expression using Western blot and qRT-PCR.
- Evaluation of cPDS and BIRC3 effects on apoptosis via flow cytometry and Annexin V-FITC staining.
- In vivo studies using a nude mouse model to assess tumor formation.
Main Results:
- cPDS significantly inhibited HCC cell proliferation and migration.
- cPDS altered BIRC3 expression, increasing mRNA but decreasing protein levels.
- BIRC3 overexpression promoted HCC cell proliferation and tumor growth in vivo.
- cPDS induced apoptosis by counteracting BIRC3-mediated anti-apoptotic effects.
Conclusions:
- cPDS demonstrates significant tumor-inhibitory properties in HCC.
- The mechanism involves regulating BIRC3 expression and promoting apoptosis.
- cPDS represents a promising therapeutic agent for HCC treatment.
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