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Updated: Jan 15, 2026
The Use of Reverse Phase Protein Arrays RPPA to Explore Protein Expression Variation within Individual Renal Cell Cancers
Published on: January 22, 2013
Integrative multi-omics analysis and experimental validation reveal centromere protein W as a potential therapeutic
Jun Li1, Ruizhen Huang1, Jie Tian2
1Department of Urology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, China.
Abstract:
Renal cell carcinoma, particularly kidney renal clear cell carcinoma (KIRC), remains a highly aggressive tumor type characterized by poor clinical outcomes and a lack of reliable molecular markers. In this study, we applied a comprehensive analytical pipeline-combining differential gene expression analysis, weighted gene co-expression network analysis (WGCNA), LASSO regression, and Random Forest modeling-based on the GSE53757 dataset to identify key regulatory genes, ultimately prioritizing CENPW for further investigation. Subsequent validation using TCGA and GTEx datasets confirmed that CENPW expression is markedly elevated in KIRC and is strongly correlated with unfavorable pathological features and reduced patient survival. Functional assays demonstrated that silencing CENPW inhibited KIRC cell proliferation, migration, invasion, and in vivo tumor growth. Notably, these effects were accompanied by increased PD-L1 and E-cadherin expression, implicating CENPW in the regulation of immune responses and epithelial-mesenchymal transition. Furthermore, predictive modeling and molecular docking revealed that tumors with elevated CENPW levels exhibited enhanced sensitivity to targeted therapies such as OSU-03012 and rapamycin. Collectively, our findings indicate that CENPW acts as a potential oncogenic regulator in KIRC, influencing both immune pathways and therapeutic responsiveness, and may serve as a novel biomarker and treatment target.
Insights
CENPW is a key gene driving kidney renal clear cell carcinoma (KIRC) progression and poor survival. Inhibiting CENPW reduces tumor growth and enhances sensitivity to targeted therapies, suggesting it as a novel KIRC biomarker and treatment target.
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- Kidney renal clear cell carcinoma (KIRC) is an aggressive cancer with poor prognosis.
- There is a critical need for reliable molecular markers and therapeutic targets in KIRC.
Purpose of the Study:
- To identify key regulatory genes in KIRC using integrated bioinformatics analysis.
- To investigate the role of CENPW in KIRC progression and its potential as a therapeutic target.
Main Methods:
- Differential gene expression analysis, WGCNA, LASSO regression, and Random Forest modeling on GSE53757 dataset.
- Validation of CENPW expression using TCGA and GTEx datasets.
- Functional assays (gene silencing) and in vivo tumor growth studies.
- Analysis of PD-L1, E-cadherin expression, and predictive modeling for targeted therapy sensitivity.
Main Results:
- CENPW expression is significantly elevated in KIRC and correlates with adverse pathological features and reduced survival.
- Silencing CENPW inhibits KIRC cell proliferation, migration, invasion, and in vivo tumor growth.
- CENPW downregulation increases PD-L1 and E-cadherin expression, impacting immune response and epithelial-mesenchymal transition.
- Elevated CENPW predicts enhanced sensitivity to targeted therapies like OSU-03012 and rapamycin.
Conclusions:
- CENPW is an oncogenic driver in KIRC, influencing tumor progression, immune evasion, and therapeutic response.
- CENPW represents a promising novel biomarker and therapeutic target for KIRC management.
