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Study reveals mechanism of lung-cancer drug resistance
Date:1/19/2012

Cancer Genetics program and a member of the OSUCCC James Molecular Biology and Cancer Genetics program.

First author Michela Garofalo notes that stratifying NSCLC patients based on MET expression or the expression of miRNAs regulated by MET might allow for individualization of treatment.

"Such a strategy could improve treatment efficacy and patient quality of life by sparing patients from the side effects of treatments that are likely to fail," says Garofalo, who is a research scientist in Croce's laboratory at the OSUCCC James.

For this study, Croce, Garofalo and their colleagues used lung cancer cell lines, animal models and analysis of human NSCLC tissue. Key technical findings include the following:

  • Both EGFR and MET control miR-30b, miR30c, miR-221, and miR-222. These miRNAs are oncogenic; they inhibit pro-apoptotic genes.
  • Overexpression of the four oncogenic miRNAs rendered gefitinib-sensitive cells resistant to treatment; inhibiting the four enhanced gefitinib sensitivity and blocked NSCLC tumor growth in an animal model.
  • MET alone controls levels of miR-103 and miR-203, which have a tumor-suppressor function. Forcing their expression enhanced gefitinib sensitivity and blocked NSCLC tumor growth in an animal model.


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Contact: Darrell E. Ward
Darrell.Ward@osumc.edu
614-293-3737
Ohio State University Medical Center
Source:Eurekalert

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