Centromere protein K enhances the activation of YAP1/TAZ signal cascade to drive the progression of clear cell renal cell carcinoma
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View abstract on PubMed
Summary
This summary is machine-generated.Centromere protein K (CENPK) is highly expressed in clear cell renal cell carcinoma (ccRCC), promoting cancer progression. Inhibiting CENPK suppressed ccRCC cell malignancy and tumor formation, suggesting CENPK as a potential therapeutic target.
Area Of Science
- Oncology
- Molecular Biology
- Genetics
Background
- Centromere protein K (CENPK) is implicated in various cancers.
- Its role in clear cell renal cell carcinoma (ccRCC) is currently unknown.
- Understanding CENPK's function in ccRCC is crucial for developing new treatments.
Purpose Of The Study
- To investigate the expression, clinical significance, biological functions, and regulatory mechanisms of CENPK in ccRCC.
- To determine if CENPK can serve as a therapeutic target for ccRCC.
Main Methods
- Analysis of The Cancer Genome Atlas (TCGA) RNA-seq data.
- Validation using clinical ccRCC samples.
- In vitro cellular functional experiments (e.g., knockdown, knockout).
- Gene Set Enrichment Analysis (GSEA).
- In vivo tumor formation assays in nude mice.
Main Results
- CENPK is highly expressed in ccRCC, correlating with advanced stage, high grade, and poor clinical outcome.
- CENPK knockdown inhibited ccRCC cell proliferation, migration, and invasion.
- CENPK regulates ccRCC progression via the Hippo-YAP1/TAZ signaling pathway.
- CENPK overexpression promoted tumor growth, which was attenuated in YAP1 knockout cells.
- Reduced CENPK expression diminished tumor formation in vivo.
Conclusions
- CENPK plays a significant role in ccRCC pathogenesis and progression.
- CENPK acts through the Hippo-YAP1/TAZ pathway to drive ccRCC malignancy.
- CENPK represents a promising therapeutic target for ccRCC treatment.
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