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RPL35A Downregulation Suppresses Hepatocellular Carcinoma Cell Proliferation via NCAPG2 Inactivation
Liang Chen1, Yujie Lin2, Yu Lai3
1Department of Intensive Care Unit, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Background:
Hepatocellular carcinoma (HCC) is a highly aggressive cancer with a poor prognosis. The molecular mechanisms underlying HCC progression remain poorly understood, prompting the need for novel therapeutic targets. RPL35A, a component of the 60S large ribosomal subunit, is a ribosomal protein involved in ribosome biogenesis and protein synthesis. Beyond its canonical role, increasing evidence suggests that ribosomal proteins such as RPL35A may also exert extraribosomal functions that contribute to tumorigenesis.
Methods:
We investigated RPL35A expression in HCC using tissue samples and cell lines. RPL35A levels were correlated with clinicopathological features and prognosis in HCC patients. In vitro, we manipulated RPL35A expression in HCC cells using shRNA lentiviral vectors and assessed its effects on cell proliferation, migration and apoptosis. In vivo, we evaluated tumor growth using xenograft models. Gene expression analysis was conducted to identify downstream targets of RPL35A.
Results:
RPL35A was significantly overexpressed in HCC tissues compared to normal liver, correlating with advanced disease stages and poorer prognosis. Knockdown of RPL35A in HCC cells inhibited cell proliferation, migration and invasion, while promoting apoptosis. In vivo, RPL35A silencing reduced tumor growth and size. Gene expression analysis identified NCAPG2 as a key downstream target of RPL35A. NCAPG2 expression was upregulated in HCC, and its knockdown reversed the oncogenic effects of RPL35A. Moreover, RPL35A overexpression increased NCAPG2 levels, promoting tumor progression. These findings suggest that the RPL35A/NCAPG2 axis is crucial in HCC development.
Conclusions:
High expression of RPL35A is linked to poor prognosis in hepatocellular carcinoma. The regulation of NCAPG2 by RPL35A may represent a critical mechanism underlying RPL35A-driven tumor progression. Targeting the RPL35A/NCAPG2 pathway may offer a promising therapeutic strategy for HCC treatment.
Insights
High levels of ribosomal protein RPL35A indicate poor prognosis in hepatocellular carcinoma (HCC). Targeting the RPL35A/NCAPG2 pathway offers a potential new treatment strategy for HCC.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Hepatocellular carcinoma (HCC) is an aggressive cancer with limited treatment options.
- Understanding the molecular drivers of HCC is crucial for developing novel therapies.
- Ribosomal proteins, like RPL35A, may have extraribosomal roles in cancer progression.
Purpose of the Study:
- To investigate the role of RPL35A in hepatocellular carcinoma (HCC).
- To identify downstream targets and mechanisms of RPL35A in HCC.
- To evaluate the therapeutic potential of targeting the RPL35A pathway in HCC.
Main Methods:
- Assessed RPL35A expression in HCC tissues and cell lines.
- Correlated RPL35A levels with patient prognosis and clinicopathological features.
- Manipulated RPL35A expression in vitro and in vivo to assess its impact on HCC progression.
- Utilized gene expression analysis to identify downstream targets of RPL35A.
Main Results:
- RPL35A was significantly overexpressed in HCC, correlating with advanced stages and poor prognosis.
- RPL35A knockdown inhibited HCC cell proliferation, migration, and invasion, while promoting apoptosis.
- RPL35A silencing reduced tumor growth in vivo.
- NCAPG2 was identified as a key downstream target, with its upregulation by RPL35A driving HCC progression.
Conclusions:
- Elevated RPL35A expression is a marker of poor prognosis in HCC.
- The RPL35A-NCAPG2 axis plays a critical role in HCC development and progression.
- Targeting the RPL35A/NCAPG2 pathway presents a promising therapeutic strategy for HCC.
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