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CDCA5-EEF1A1 interaction promotes progression of clear cell renal cell carcinoma by regulating mTOR signaling.
Wang, Xun; Shi, An; Liu, Jie; Kong, Wen; Huang, Yiran; Xue, Wei; Yang, Fan; Huang, Jiwei.
Afiliação
  • Wang X; Department of Urology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China.
  • Shi A; Department of Critical Care Medicine, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China.
  • Liu J; Department of Pharmacy, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China.
  • Kong W; Department of Urology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China.
  • Huang Y; Department of Urology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China.
  • Xue W; Department of Urology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China.
  • Yang F; Department of Pharmacy, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China. yang-fan@sjtu.edu.cn.
  • Huang J; Department of Urology, Renji Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200127, China. huangjiwei@renji.com.
Cancer Cell Int ; 24(1): 147, 2024 Apr 24.
Article em En | MEDLINE | ID: mdl-38658931
ABSTRACT

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.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Ano de publicação: 2024 Tipo de documento: Article