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Role of Sam68 in Sunitinib induced renal cell carcinoma apoptosis

Zeshen Wu1,2,3, Yulu Peng1,2,3, Longbin Xiong1,2,3

  • 1Department of Urology, Sun Yat-sen University Cancer Center, Guangzhou, China.

Cancer Medicine
|April 27, 2022
PubMed

Insights

Sam68 protein levels influence treatment outcomes for metastatic renal cell carcinoma (RCC). Higher Sam68 expression enhances sunitinib-induced apoptosis, suggesting it may predict patient response to this targeted therapy.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Sunitinib is a first-line targeted therapy for metastatic renal cell carcinoma (RCC), acting via antiangiogenesis and proapoptosis.
  • Sam68 (Src-associated in mitosis, 68 KDa) is implicated in cellular apoptosis pathways.

Purpose of the Study:

  • To investigate the role of Sam68 in mediating RCC cell apoptosis and its impact on sunitinib sensitivity.
  • To determine if Sam68 expression levels can serve as a predictive biomarker for sunitinib efficacy in ccRCC patients.

Main Methods:

  • Immunohistochemical staining of tumor tissues to compare Sam68 expression in sunitinib-sensitive versus resistant RCC.
  • In vitro experiments assessing sunitinib-induced apoptosis and Sam68 expression (total and phosphorylated) in RCC cells.
  • In vivo studies using xenograft models with Sam68-knockdown and control groups treated with sunitinib.

Main Results:

  • Sam68 expression was significantly higher in sunitinib-sensitive RCC tissues compared to resistant tissues.
  • Sunitinib induced RCC cell apoptosis in a dose-dependent manner, concurrently inhibiting Sam68 expression.
  • Downregulating Sam68 reduced sunitinib-induced apoptosis, while upregulating Sam68 enhanced it. Xenograft tumors in Sam68-knockdown mice showed less shrinkage with sunitinib treatment.

Conclusions:

  • Sam68 expression is correlated with ccRCC patient sensitivity to sunitinib.
  • Sam68 promotes sunitinib-induced apoptosis in RCC cells.
  • Sam68 levels may serve as a predictive biomarker for sunitinib response in ccRCC.
Keywords:
Sam68cell apoptosisdrug sensitivityrenal cell carcinomasunitinib

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