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WT1 enhances proliferation and impedes apoptosis in KRAS mutant NSCLC via targeting cMyc

Chen Wu1, Sihan Wang, Caihua Xu

  • 1Department of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Changzhou, China.

Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology
|January 24, 2015
PubMed
Abstract

Insights

WT1 and c-Myc expression are crucial for survival in KRAS mutant non-small cell lung cancer (NSCLC). Targeting WT1 and c-Myc may offer new therapeutic strategies for KRAS mutant NSCLC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • A novel link between oncogenic KRAS signaling and WT1 was recently identified.
  • Investigated the roles of WT1 and KRAS in cancer cell proliferation and apoptosis.

Purpose of the Study:

  • To investigate the role of WT1 and KRAS in proliferation and apoptosis in non-small cell lung cancer (NSCLC).
  • To explore the therapeutic potential of targeting WT1 and c-Myc in KRAS mutant NSCLC.

Main Methods:

  • KRAS mutations and WT1 (cMyc) expression analyzed in 77 NSCLC patients using Sanger sequencing and real-time PCR.
  • WT1 overexpression and knockdown performed in cell lines; proliferation and apoptosis assays conducted.
  • WT1's effect on the c-Myc promoter validated using dual luciferase reporter and ChIP-PCR assays.

Main Results:

  • KRAS mutations negatively impacted overall survival (OS).
  • High WT1 and c-Myc expression correlated with poor OS in the KRAS mutant subgroup.
  • WT1 promotes proliferation and inhibits apoptosis in KRAS mutant NSCLC cells, partly by activating the c-Myc promoter.

Conclusions:

  • WT1 and c-Myc expression are vital for survival in KRAS mutant tumors.
  • Targeting WT1 and c-Myc presents potential therapeutic strategies for KRAS mutant NSCLC.

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