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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

STI1 promotes glioma proliferation through AUPK and PI3K pathways

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Erlich, Rafael B. ; Kahn, Suzana A. ; Lima, Flávia R. S. ; Muras, Angelita G. ; Martins, Rodrigo A. P. ; Linden, Rafael ; Chiarini, Luciana B. ; Martins, Vilma R. [8] ; Moura Neto, Vivaldo
Total Authors: 9
Document type: Journal article
Source: Glia; v. 55, n. 16, p. 1690-1698, Dec. 2007.
Field of knowledge: Biological Sciences - Biochemistry

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 (PrPC), 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 PrPC 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. (AU)

FAPESP's process: 03/13189-2 - The role of celular prion protein in physiological and pathological processes II
Grantee:Vilma Regina Martins
Support type: Research Projects - Thematic Grants