CDCA5-EEF1A1 interaction promotes progression of clear cell renal cell carcinoma by regulating mTOR signaling

Xun Wang1, An Shi2, Jie Liu3

  • 1Department of Urology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China.

PubMed
Abstract

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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