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Molecular and Immunologic Techniques in a Genetically Engineered Mouse Model of Gastrointestinal Stromal Tumor
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[Expression of MDR1 and KIT in imatinib-resistant gastrointestinal stromal tumor cells]

Jing-lei Liu1, Jing Qin, Li-qing Yao

  • 1Department of General Surgery, Zhongshan Hospital, Fudan Universtity, Shanghai 200032, China.

Zhonghua Wei Chang Wai Ke Za Zhi = Chinese Journal of Gastrointestinal Surgery
|July 27, 2010
PubMed
Abstract

Insights

Over-expression of the MDR1 gene, which encodes P-glycoprotein, is linked to imatinib resistance in gastrointestinal stromal tumor (GIST) cells. The KIT gene and its protein CD117 do not appear to play a role in this resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Gastrointestinal stromal tumors (GIST) are often treated with imatinib, a tyrosine kinase inhibitor.
  • Resistance to imatinib is a significant clinical challenge in GIST treatment.
  • The mechanisms underlying imatinib resistance in GIST are not fully understood.

Purpose of the Study:

  • To investigate the association between imatinib resistance and the expression of MDR1 and KIT genes in GIST cells.
  • To determine the role of P-glycoprotein (P-gp) and CD117 in imatinib resistance.

Main Methods:

  • Quantitative real-time PCR (RT-PCR) was used to measure MDR1 and KIT mRNA levels.
  • Immunocytochemistry and Western blot analyses were performed to assess P-gp and CD117 protein expression.
  • Experiments utilized imatinib-resistant (GIST882-R) and imatinib-sensitive (GIST882-S) GIST cell lines.

Main Results:

  • MDR1 mRNA expression was significantly higher in GIST882-R cells compared to GIST882-S cells (P<0.05).
  • P-gp protein levels were significantly elevated in GIST882-R cells versus GIST882-S cells (P<0.05).
  • No significant differences in KIT mRNA or CD117 protein expression were observed between the resistant and sensitive cell lines (P>0.05).

Conclusions:

  • Over-expression of the MDR1 gene and its protein product, P-gp, is strongly associated with imatinib resistance in GIST.
  • The KIT gene and CD117 protein are unlikely to be involved in the development of imatinib resistance in this GIST model.
  • These findings suggest that targeting MDR1/P-gp could be a potential strategy to overcome imatinib resistance in GIST.

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