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Critical role for transcriptional repressor Snail2 in transformation by oncogenic RAS in colorectal carcinoma cells

Y Wang1, V N Ngo, M Marani

  • 1Signal Transduction Laboratory, Cancer Research UK London Research Institute, London, UK.

Oncogene
|June 22, 2010
PubMed

Insights

Activating KRAS mutations drive cancer. Researchers found Snail2 is essential for survival in KRAS-mutant cancer cells that underwent epithelial-mesenchymal transition (EMT), suggesting Snail2 as a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Activating mutations in the KRAS gene are common in human cancers.
  • Epithelial-mesenchymal transition (EMT) is a process frequently observed in advanced tumors and is promoted by RAS pathway activation.

Purpose of the Study:

  • To identify synthetic lethal interactions in cancer cells with mutant KRAS.
  • To investigate the role of Snail2 in KRAS-mutant cancer survival and EMT.

Main Methods:

  • Conducted a large-scale screen using an inducible short hairpin RNA interference library.
  • Utilized isogenic paired colon cancer cell lines differing by a single allele of mutant KRAS.

Main Results:

  • Identified Snail2 (encoded by SNAI2 gene) as selectively required for long-term survival of KRAS-mutant cancer cells that underwent EMT.
  • Demonstrated that Snail2 expression is regulated by the RAS pathway and is essential for EMT.

Conclusions:

  • Snail2 is crucial for the survival of KRAS-mutant cancers with EMT.
  • Snail2 represents a potential therapeutic target for epithelial cancers with mutant RAS, EMT, chemoresistance, and radioresistance.

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