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Evi1 is a survival factor which conveys resistance to both TGFbeta- and taxol-mediated cell death via PI3K/AKT

Y Liu1, L Chen, T C Ko

  • 1Department of Cancer Biology, Mayo Clinic Comprehensive Cancer Center, Jacksonville, FL 32224, USA.

Oncogene
|February 8, 2006
PubMed

Insights

The oncogene Evi1 promotes survival in intestinal and colon cancer cells by activating PI3K/AKT signaling, conferring resistance to apoptosis. This finding is crucial for understanding Evi1

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • The oncogene Evi1's role in epithelial cancers and its effect on TGFbeta signaling are not fully understood.
  • Evi1's transforming potential in hematopoietic cells is linked to TGFbeta signaling inhibition.

Purpose of the Study:

  • To investigate the effects of Evi1 on TGFbeta signaling and apoptosis in intestinal epithelial cells.
  • To determine Evi1's role in colon cancer cell survival and response to apoptosis.

Main Methods:

  • Stable expression of Evi1 in intestinal epithelial cells.
  • Analysis of TGFbeta target gene induction, cellular adhesion, epithelial-mesenchymal transition, and growth inhibition.
  • Investigating Evi1's effect on TGFbeta- and taxol-mediated apoptosis.
  • Evi1 gene amplification analysis in colon cancer cell lines.
  • Evi1 knockdown using siRNA in HT-29 colon cancer cells.

Main Results:

  • Evi1 inhibited some Smad3-dependent TGFbeta target genes but not cellular adhesion or epithelial-mesenchymal transition.
  • Evi1 did not inhibit TGFbeta-mediated growth inhibition but suppressed TGFbeta- and taxol-mediated apoptosis via PI3K/AKT activation.
  • Evi1 overexpression, associated with gene amplification, was observed in colon cancer cell lines.
  • Evi1 knockdown in HT-29 cells reduced AKT phosphorylation and increased sensitivity to taxol-induced apoptosis.

Conclusions:

  • Evi1 acts as a survival gene in intestinal epithelial and colon cancer cells.
  • Evi1 activates PI3K/AKT signaling, providing resistance to physiological and therapeutic apoptotic stimuli.
  • Targeting Evi1 may offer a therapeutic strategy for colon cancer.

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