Abstract
Abstract Caveolin-1 is an essential structural constituent of caveolae implicated in mitogenic signalling, oncogenesis, angiogenesis, neurodegenerative diseases and senescence. Its role as a tumor suppressor gene or as a tumor promoter seems to strictly depend on cell type and tumor stage/grade. The high expression of caveolin-1 in some tumors in vivo is associated with increased tumor aggressiveness, metastatic potential and suppression of apoptosis. In the present study we investigated the role of Caveolin-1 in human glioblastoma cells proliferation, in which we found cav-1 expressed at high levels (A172, CRS-A2, LI). Results show that siRNA-mediated down-regulation of Cav-1 caused stable arrest of proliferation in each cell line. A marked reduction of cyclin D1 and of CDK4 expression was evident in the cells transfected with Cav-1 siRNA and consequently of phosphoRb. Furthermore, a significant decrease of the expression of Src and p38α and of their down-stream effector STAT3 was evident. Together, these findings indicate that Cav-1 silencing induces an arrest of tumor cells proliferation in vitro by a new inhibitory pathway in glioblastoma multiforme, the most aggressive of the primary central nervous system tumors, and provide new insights into the molecular mechanisms underlying the pro-survival and tumor-promoting functions of Cav-1. Grants from MIUR (RFO, PRIN), Roberto Pallotti's Legacy for Cancer Research, Cornelia Pallotti's Legacy for Cancer Research, University of Bologna, Italy Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 900. doi:1538-7445.AM2012-900
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