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Updated: Jun 28, 2025

Comparing Metastatic Clear Cell Renal Cell Carcinoma Model Established in Mouse Kidney and on Chicken Chorioallantoic Membrane
Published on: February 8, 2020
CDCA5-EEF1A1 interaction promotes progression of clear cell renal cell carcinoma by regulating mTOR signaling
1Department of Urology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China.
Background:
Cell division cycle associated 5 (CDCA5) plays ontogenetic role in various human cancers. However, its specific function and regulatory mechanism in ccRCC remain uncertain.
Methods:
Immunohistochemistry and western blots were performed to investigate the expression of CDCA5 in ccRCC tissues. Genetic knockdown and upregulation of CDCA5 were performed to investigate its functional roles in ccRCC proliferation, migration, apoptosis and sunitinib resistance. Furthermore, Co-IP assay and LC-MS/MS were performed to investigate the underlying mechanisms.
Results:
We found that CDCA5 expression is frequently upregulated in ccRCC tumors and is associated with poor prognosis of ccRCC patients. Functionally, CDCA5 promotes proliferation, migration, and sunitinib resistance, while inhibiting apoptosis in ccRCC cells. In vivo mouse xenograft model confirms that silencing of CDCA5 drastically inhibits the growth of ccRCC. Mechanistically, we discovered that CDCA5 interacts with Eukaryotic Translation Elongation Factor 1 Alpha 1 (EEF1A1) to regulate mTOR signaling pathway, thereby promoting ccRCC progression.
Conclusions:
Taken together, our results demonstrate the significant role of CDCA5 in ccRCC progression. The findings may provide insights for the development of new treatment strategies targeting CDCA5 for ccRCC patients.
Insights
Cell division cycle associated 5 (CDCA5) promotes kidney cancer progression by enhancing cell growth and resistance to sunitinib. Targeting CDCA5 may offer new therapeutic strategies for clear cell renal cell carcinoma (ccRCC).
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Cell division cycle associated 5 (CDCA5) has an established role in various human cancers.
- The specific function and regulatory mechanisms of CDCA5 in clear cell renal cell carcinoma (ccRCC) are not well understood.
Purpose of the Study:
- To investigate the expression, function, and underlying mechanisms of CDCA5 in ccRCC.
- To explore the potential of CDCA5 as a therapeutic target for ccRCC.
Main Methods:
- Immunohistochemistry and western blots to assess CDCA5 expression in ccRCC tissues.
- Genetic manipulation (knockdown/upregulation) of CDCA5 to study its effects on ccRCC cell proliferation, migration, apoptosis, and sunitinib resistance.
- Co-immunoprecipitation (Co-IP) and liquid chromatography-tandem mass spectrometry (LC-MS/MS) to elucidate molecular mechanisms.
- In vivo mouse xenograft models to confirm functional roles.
Main Results:
- CDCA5 is frequently upregulated in ccRCC tumors and correlates with poor patient prognosis.
- CDCA5 promotes ccRCC cell proliferation and migration, inhibits apoptosis, and enhances resistance to sunitinib.
- Silencing CDCA5 significantly inhibits ccRCC tumor growth in vivo.
- CDCA5 interacts with Eukaryotic Translation Elongation Factor 1 Alpha 1 (EEF1A1) to regulate the mTOR signaling pathway, driving ccRCC progression.
Conclusions:
- CDCA5 plays a critical role in ccRCC progression.
- Targeting CDCA5 presents a promising avenue for developing novel therapeutic strategies for ccRCC patients.
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