This Article Full Text Full Text (PDF) Supplementary Data Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Muders, M. H. Articles by Mukhopadhyay, D. Search for Related Content PubMed PubMed Citation Articles by Muders, M. H. Articles by Mukhopadhyay, D.

Expression and Regulatory Role of GAIP-Interacting Protein GIPC in Pancreatic Adenocarcinoma

¹ Department of Biochemistry and Molecular Biology and Mayo Clinic Cancer Center; Departments of ² Pathology and ³ Medicine, Mayo Clinic College of Medicine, Rochester, Minnesota

Requests for reprints: Debabrata Mukhopadhyay, Department of Biochemistry and Molecular Biology, Gugg 1401A, Mayo Clinic College of Medicine, 200 First Street Southwest, Rochester MN 55905. Phone: 507-538-3581; Fax: 507-284-1767; E-mail: mukhopadhyay.debabrata{at}mayo.edu.

Regulator of G-protein signaling–GAIP-interacting protein COOH terminus (GIPC) is involved in protein trafficking, endocytosis, and receptor clustering and is associated with insulin-like growth factor I receptor (IGF-IR), a receptor important for proliferation and anchorage-independent growth. Here, we described GIPC expression in different human pancreatic adenocarcinoma (PCA) cell lines and we examined the role of GIPC in the regulation of IGF-IR protein levels in PCA. Interestingly, inhibition of GIPC expression by RNA interference led to reduced IGF-IR protein levels and a subsequent decrease in proliferation of PCA cells. We also determined that the PDZ domain of GIPC is essential for the post-translational regulation and the binding of IGF-IR. The importance of GIPC in pancreatic cancer development and progression is supported by tissue microarray data of 300 pancreatic cancer specimens where GIPC is highly expressed in PCA. Taken together, our data suggest that GIPC is a central molecule for the stability of IGF-IR and could be a target for future therapy. (Cancer Res 2006; 66(21): 10264-8)

This article has been cited by other articles:

				M. H. Muders, P. K. Vohra, S. K. Dutta, E. Wang, Y. Ikeda, L. Wang, D. G. Udugamasooriya, A. Memic, C. N. Rupashinghe, G. B. Baretton, et al. Targeting GIPC/Synectin in Pancreatic Cancer Inhibits Tumor Growth Clin. Cancer Res., June 15, 2009; 15(12): 4095 - 4103. [Abstract] [Full Text] [PDF]

				C. Prahst, M. Heroult, A. A. Lanahan, N. Uziel, O. Kessler, N. Shraga-Heled, M. Simons, G. Neufeld, and H. G. Augustin Neuropilin-1-VEGFR-2 Complexing Requires the PDZ-binding Domain of Neuropilin-1 J. Biol. Chem., September 12, 2008; 283(37): 25110 - 25114. [Abstract] [Full Text] [PDF]