Enhanced expression of the insulin receptor substrate-2 docking protein in human pancreatic cancer - PubMed (original) (raw)
. 1998 Oct 1;58(19):4250-4.
Affiliations
- PMID: 9766646
Enhanced expression of the insulin receptor substrate-2 docking protein in human pancreatic cancer
M Kornmann et al. Cancer Res. 1998.
Abstract
Insulin receptor substrate-2 (IRS-2) is a multisite docking protein implicated in mitogenic signaling after activation of the insulin and insulin-like growth factor (IGF)-I receptors. In the present study, we characterized IRS-2 expression and function in human pancreatic cancer. IRS-2 mRNA and protein were expressed in ASPC-1 and COLO-357 human pancreatic cancer cell lines. Insulin, IGF-I, and IGF-II enhanced the growth of both cell lines, stimulated tyrosine phosphorylation of IRS-2, and increased IRS-2-associated phosphatidylinositol (PI) 3-kinase activity. The mitogenic effects of insulin, IGF-I, and IGF-II were markedly attenuated by the PI 3-kinase inhibitor LY 294002. Northern blot analysis of total RNA extracted from normal and cancerous tissues revealed that IRS-2 mRNA levels were increased in the cancer tissues (P = 0.032). In the normal pancreas, IRS-2 immunoreactivity was present at low levels in some ductal and acinar cells and at moderate levels in a heterogeneous pattern in all of the endocrine islets. In the pancreatic cancers, IRS-2 was abundant in the ductal-like cancer cells. These findings indicate that IRS-2 is overexpressed in human pancreatic cancer and suggest that it may contribute to enhanced mitogenic signaling via the PI 3-kinase pathway, thereby leading to excessive growth stimulation in this malignancy.
Similar articles
- Increased expression of insulin receptor substrate-1 in human pancreatic cancer.
Bergmann U, Funatomi H, Kornmann M, Beger HG, Korc M. Bergmann U, et al. Biochem Biophys Res Commun. 1996 Mar 27;220(3):886-90. doi: 10.1006/bbrc.1996.0500. Biochem Biophys Res Commun. 1996. PMID: 8607861 - Progesterone receptor-B regulation of insulin-like growth factor-stimulated cell migration in breast cancer cells via insulin receptor substrate-2.
Ibrahim YH, Byron SA, Cui X, Lee AV, Yee D. Ibrahim YH, et al. Mol Cancer Res. 2008 Sep;6(9):1491-8. doi: 10.1158/1541-7786.MCR-07-2173. Mol Cancer Res. 2008. PMID: 18819936 Free PMC article. - Insulin-like growth factor-1 (IGF-1) receptor-insulin receptor substrate complexes in the uterus. Altered signaling response to estradiol in the IGF-1(m/m) mouse.
Richards RG, Walker MP, Sebastian J, DiAugustine RP. Richards RG, et al. J Biol Chem. 1998 May 8;273(19):11962-9. doi: 10.1074/jbc.273.19.11962. J Biol Chem. 1998. PMID: 9565625
Cited by
- Involvement of IL-4, IL-13 and Their Receptors in Pancreatic Cancer.
Shi J, Song X, Traub B, Luxenhofer M, Kornmann M. Shi J, et al. Int J Mol Sci. 2021 Mar 15;22(6):2998. doi: 10.3390/ijms22062998. Int J Mol Sci. 2021. PMID: 33804263 Free PMC article. Review. - Diabetes and risk of cancer.
Habib SL, Rojna M. Habib SL, et al. ISRN Oncol. 2013;2013:583786. doi: 10.1155/2013/583786. Epub 2013 Feb 7. ISRN Oncol. 2013. PMID: 23476808 Free PMC article. - Interleukin-4 enhances proliferation of human pancreatic cancer cells: evidence for autocrine and paracrine actions.
Prokopchuk O, Liu Y, Henne-Bruns D, Kornmann M. Prokopchuk O, et al. Br J Cancer. 2005 Mar 14;92(5):921-8. doi: 10.1038/sj.bjc.6602416. Br J Cancer. 2005. PMID: 15714203 Free PMC article. - Expression and function of the insulin receptor substrate proteins in cancer.
Mardilovich K, Pankratz SL, Shaw LM. Mardilovich K, et al. Cell Commun Signal. 2009 Jun 17;7:14. doi: 10.1186/1478-811X-7-14. Cell Commun Signal. 2009. PMID: 19534786 Free PMC article. - Differential Expression of IRS-1 and IRS-2 in Uterine Leiomyosarcomas with Distinct Oncogenic Phenotypes: Lack of Correlation with Downstream Signaling Events.
Colombatti A, Russo P, Cervi M, Bogetto L, Wassermann B, Mainiero F, Spessotto P. Colombatti A, et al. Sarcoma. 2002;6(3):89-96. doi: 10.1080/1357714021000065387. Sarcoma. 2002. PMID: 18521338 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Medical
Research Materials
Miscellaneous