STI1 promotes glioma proliferation through MAPK and PI3K pathways
- PMID: 17886292
- DOI: 10.1002/glia.20579
STI1 promotes glioma proliferation through MAPK and PI3K pathways
Abstract
Gliomas are tumors derived from glia or their precursors within the central nervous system. Clinically, gliomas are divided into four grades and the glioblastoma multiforme (GBM), also referred as grade IV astrocytoma, is the most aggressive and the most common glioma in humans. The prognosis for patients with GBM remains dismal, with a median survival of 9-12 months. Despite their striking heterogeneity, common alterations in specific cellular signal transduction pathways occur within most GBMs. Previous work from our group identified the co-chaperone stress-inducible protein 1 (STI1) as a cell surface ligand for cellular prion (PrP(C)), which leads to the activation of several signal transduction pathways, some of which modulate cell survival. In the present work, we used thymidine incorporation assays to investigate the effect of STI1 upon proliferation of the human glioblastoma-derived cell line A172. Here we report that STI1 is secreted by and induces proliferation in tumor cells, an effect that is modulated by the Erk and PI3K pathways, and that, in contrast to glioma cells, STI1 does not induce proliferation of normal glia. In addition, our data suggest the involvement of PrP(C) in STI1-induced proliferation of A172 cells. These results provide initial evidence of a new functional role for STI1 on the physiology of human gliomas, and may lead to the identification of new therapeutic targets in these tumors.
(c) 2007 Wiley-Liss, Inc.
Similar articles
-
Prion protein and its ligand stress inducible protein 1 regulate astrocyte development.Glia. 2009 Oct;57(13):1439-49. doi: 10.1002/glia.20861. Glia. 2009. PMID: 19243016
-
Microglial stress inducible protein 1 promotes proliferation and migration in human glioblastoma cells.Neuroscience. 2012 Jan 3;200:130-41. doi: 10.1016/j.neuroscience.2011.10.025. Epub 2011 Oct 25. Neuroscience. 2012. PMID: 22062133
-
Hop/STI1 modulates retinal proliferation and cell death independent of PrPC.Biochem Biophys Res Commun. 2007 Sep 21;361(2):474-80. doi: 10.1016/j.bbrc.2007.07.038. Epub 2007 Jul 18. Biochem Biophys Res Commun. 2007. PMID: 17651690
-
Targeting malignant glioma survival signalling to improve clinical outcomes.J Clin Neurosci. 2007 Apr;14(4):301-8. doi: 10.1016/j.jocn.2006.11.005. Epub 2007 Feb 1. J Clin Neurosci. 2007. PMID: 17276069 Review.
-
[Histological and molecular classification of gliomas].Rev Neurol (Paris). 2008 Jun-Jul;164(6-7):505-15. doi: 10.1016/j.neurol.2008.03.011. Epub 2008 Jun 10. Rev Neurol (Paris). 2008. PMID: 18565348 Review. French.
Cited by
-
The Role of Cellular Prion Protein in Glioma Tumorigenesis Could Be through the Autophagic Mechanisms: A Narrative Review.Int J Mol Sci. 2023 Jan 11;24(2):1405. doi: 10.3390/ijms24021405. Int J Mol Sci. 2023. PMID: 36674920 Free PMC article. Review.
-
Glioma-derived LRIG3 interacts with NETO2 in tumor-associated macrophages to modulate microenvironment and suppress tumor growth.Cell Death Dis. 2023 Jan 13;14(1):28. doi: 10.1038/s41419-023-05555-z. Cell Death Dis. 2023. PMID: 36639372 Free PMC article.
-
With or without You: Co-Chaperones Mediate Health and Disease by Modifying Chaperone Function and Protein Triage.Cells. 2021 Nov 11;10(11):3121. doi: 10.3390/cells10113121. Cells. 2021. PMID: 34831344 Free PMC article. Review.
-
The Hsp70-Hsp90 go-between Hop/Stip1/Sti1 is a proteostatic switch and may be a drug target in cancer and neurodegeneration.Cell Mol Life Sci. 2021 Dec;78(23):7257-7273. doi: 10.1007/s00018-021-03962-z. Epub 2021 Oct 22. Cell Mol Life Sci. 2021. PMID: 34677645 Free PMC article. Review.
-
Tumor-Associated Microglia and Macrophages in the Glioblastoma Microenvironment and Their Implications for Therapy.Cancers (Basel). 2021 Aug 24;13(17):4255. doi: 10.3390/cancers13174255. Cancers (Basel). 2021. PMID: 34503065 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Research Materials
Miscellaneous