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Overexpressed CacyBP/SIP leads to the suppression of growth in renal cell carcinoma

Shiren Sun1, Xiaoxuan Ning, Jie Liu

  • 1State Key Laboratory of Cancer Biology, Department of Nephrology, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi, China.

Biochemical and Biophysical Research Communications
|April 3, 2007
PubMed

Insights

Calcyclin-binding protein/Siah-1-interacting protein (CacyBP/SIP) is down-regulated in renal cell carcinoma. Overexpressing CacyBP/SIP inhibits cancer cell proliferation and tumorigenesis, suggesting its tumor-suppressive role.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Calcyclin-binding protein/Siah-1-interacting protein (CacyBP/SIP) is implicated in gastric cancer malignancy.
  • The function of CacyBP/SIP in renal cell carcinoma (RCC) is currently unknown.

Purpose of the Study:

  • To investigate the expression levels of CacyBP/SIP in human renal cancer.
  • To explore the functional role of CacyBP/SIP in regulating the malignant phenotype of renal cancer cells.

Main Methods:

  • Analysis of CacyBP/SIP protein expression in RCC tissues and cell lines.
  • Ectopic overexpression of CacyBP/SIP in A498 renal cancer cells.
  • Assessment of cell proliferation, cell cycle progression, colony formation, and tumorigenicity in nude mice.

Main Results:

  • CacyBP/SIP expression was significantly down-regulated in RCC tissues and cell lines.
  • Overexpression of CacyBP/SIP inhibited renal cancer cell proliferation and delayed cell cycle progression.
  • CacyBP/SIP suppressed colony formation and reduced tumor growth in vivo, potentially via beta-catenin/Cyclin D1 pathway.

Conclusions:

  • CacyBP/SIP acts as a tumor suppressor in renal cell carcinoma.
  • Down-regulation of CacyBP/SIP is associated with renal cancer progression.
  • CacyBP/SIP represents a potential therapeutic target for renal cancer.

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