STI1 promotes glioma proliferation through MAPK and PI3K pathways

Erlich R.B., Kahn S.A., Lima F.R.S., Muras A.G., Martins R.A.P., Linden R., Chiarini L.B., Martins V.R. and Neto V.M. (2007) STI1 promotes glioma proliferation through MAPK and PI3K pathways. GLIA, 55 16: 1690-1698. doi:10.1002/glia.20579

Author Erlich R.B.
Kahn S.A.
Lima F.R.S.
Muras A.G.
Martins R.A.P.
Linden R.
Chiarini L.B.
Martins V.R.
Neto V.M.
Title STI1 promotes glioma proliferation through MAPK and PI3K pathways
Journal name GLIA   Check publisher's open access policy
ISSN 0894-1491
Publication date 2007
Sub-type Article (original research)
DOI 10.1002/glia.20579
Volume 55
Issue 16
Start page 1690
End page 1698
Total pages 9
Subject 2403 Immunology
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 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.
Keyword Cellular prion protein
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collection: Scopus Import
Version Filter Type
Citation counts: Scopus Citation Count Cited 42 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Tue, 26 Nov 2013, 20:40:31 EST by System User