P53 Is Involved in Sunitinib Resistance and Poor Progression-free Survival After Sunitinib Treatment of Renal Cell Carcinoma

Anticancer Res. 2021 Sep;41(9):4287-4294. doi: 10.21873/anticanres.15233.

Abstract

Background/aim: Sunitinib continues to be administered as a first-line therapeutic agent in metastatic renal cell carcinoma (mRCC). This study examined the potential role of p53 in sunitinib resistance and as a predictive marker in mRCC.

Materials and methods: We analysed the effects of p53 knockout on sunitinib resistance. p53 expression in 53 mRCC patients receiving first-line sunitinib was determined immunohistochemically. We performed in silico analysis to examine the predictive value of p53 in mRCC.

Results: WST-1 assays showed that p53 knockout decreased sensitivity to sunitinib. Sunitinib and nutlin-3 together suppressed cell growth. Immunohistochemistry revealed 11 p53-positive cases among 53 patients with mRCC. Kaplan-Meier analysis showed that p53-positive cases tended to be associated with poor progression-free survival (PFS) after first-line sunitinib treatment. In the JAVELIN 101 study, TP53 mutation was significantly associated with poor PFS after sunitinib treatment.

Conclusion: p53 may be involved in sunitinib resistance and represent a valuable marker for sunitinib treatment in mRCC.

Keywords: in silico analysis; p53; renal cell carcinoma; sunitinib.

MeSH terms

  • Adult
  • Aged
  • Aged, 80 and over
  • Carcinoma, Renal Cell / drug therapy*
  • Carcinoma, Renal Cell / genetics
  • Carcinoma, Renal Cell / metabolism
  • Cell Proliferation / drug effects
  • Computer Simulation
  • Drug Resistance, Neoplasm*
  • Drug Synergism
  • Female
  • Gene Knockout Techniques
  • Humans
  • Imidazoles / pharmacology*
  • Kaplan-Meier Estimate
  • Kidney Neoplasms / drug therapy*
  • Kidney Neoplasms / genetics
  • Kidney Neoplasms / metabolism
  • Male
  • Middle Aged
  • Piperazines / pharmacology*
  • Progression-Free Survival
  • Retrospective Studies
  • Sunitinib / pharmacology*
  • Treatment Outcome
  • Tumor Suppressor Protein p53 / genetics*
  • Tumor Suppressor Protein p53 / metabolism
  • Up-Regulation* / drug effects

Substances

  • Imidazoles
  • Piperazines
  • TP53 protein, human
  • Tumor Suppressor Protein p53
  • nutlin 3
  • Sunitinib