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[Cancer Research 63, 6928-6934, October 15, 2003]
© 2003 American Association for Cancer Research

Regular Articles

Proteomic Profiling Drug-Induced Apoptosis in Non-Small Cell Lung Carcinoma

Identification of RS/DJ-1 and RhoGDI{alpha}1

Jeffrey P. MacKeigan, Casey M. Clements, John D. Lich, R. Marshall Pope, Yaacov Hod and Jenny P-Y. Ting2

Lineberger Comprehensive Cancer Center [J. P. M., C. M. C., J. D. L., J. P-Y. T.] and Departments of Microbiology and Immunology [J. P. M., C. M. C., J. D. L., J. P-Y. T.] and Biochemistry [R. M. P.], University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599, and Prostate Cancer Research Center, Department of Urology, State University of New York, Stony Brook, New York 11794 [Y. H.]

The growing knowledge of the tight connection between apoptosis and cancer has lead to an explosion of research revolving around apoptotic induction with chemotherapeutic agents and small molecule inhibitors. The chemotherapeutic agent paclitaxel (Taxol) activates mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase and, combined with MEK inhibition, synergistically enhances apoptosis. Here we implement a proteomic approach using two-dimensional gels coupled with mass spectrometry to identify proteins altered with this coordinated combination treatment. We found that the combined treatment of paclitaxel and MEK inhibitor uniquely altered the proteins RS/DJ-1 (RNA-binding regulatory subunit/DJ-1 PARK7) and RhoGDI{alpha} (Rho GDP-dissociation inhibitor {alpha}). Functional proteomic analysis by exogenous expression or short interfering RNA targeting confirmed a role in survival and apoptosis for these proteins. Analysis of primary lung tumors with matched adjacent normal tissue confirmed RS/DJ-1 overexpression in non-small cell lung carcinoma. This study shows the power of proteomic profiling coupled with functional analysis for the discovery of novel molecular targets and potential cancer cell-specific biomarkers.




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