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ERas enhances resistance to CPT-11 in gastric cancer

Eiji Kubota1, Hiromi Kataoka, Mamoru Tanaka

  • 1Department of Gastroenterology and Metabolism, Nagoya City University, Graduate School of Medical Sciences. 1 Kawasumi, Mizuho, Nagoya 467-8601, Japan.

Anticancer Research
|October 4, 2011
PubMed
Abstract

Insights

Embryonic stem cell-expressed Ras (ERas) promotes chemoresistance in gastric cancer. Targeting the phosphatidylinositol-3 kinase-protein kinase B-mammalian target of rapamycin pathway and nuclear factor-kappa B can overcome this resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Embryonic stem cell-expressed Ras (ERas) is present in human gastric cancer.
  • ERas expression is linked to gastric cancer's tumorigenicity.

Purpose of the Study:

  • To investigate the role of ERas in chemoresistance in human gastric cancer.
  • To explore the mechanisms underlying ERas-mediated chemoresistance.

Main Methods:

  • Assessed cytotoxicity of CPT-11 and mammalian target of rapamycin (mTOR) inhibitors on ERas-overexpressing gastric cancer cells.
  • Investigated ERas-induced chemoresistance mechanisms using electrophoretic mobility shift assay and PCR array.

Main Results:

  • ERas-overexpressing cells showed significant resistance to CPT-11.
  • Rapamycin treatment was cytotoxic to ERas-overexpressing cells.
  • ERas enhanced nuclear factor (NF)-κB activity and upregulated multidrug efflux transporter genes like ABCG2.

Conclusions:

  • ERas induces chemoresistance to CPT-11 through activation of the phosphatidylinositol-3 kinase-protein kinase B-mTOR pathway and NF-κB.
  • This activation leads to the upregulation of ABCG2, contributing to chemoresistance.

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