期刊
CELLULAR SIGNALLING
卷 24, 期 7, 页码 1390-1397出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2012.02.015
关键词
Caveolin-1 silencing; Metastatic lung cancer; Cyclin D1/pRb; AKT/ERK; STAT3 signaling
类别
资金
- MIUR-PRIN, Italy
- Roberto Pallotti's Legacy for Cancer Research
- Cornelia Pallotti's Legacy for Cancer Research
- RFO University of Bologna, Italy
- Interdepartmental Center for the Research on Cancer Giorgio Prodi, University of Bologna, Italy
Cav-1 is an essential structural constituent of caveolae implicated in mitogenic signaling, 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 Cav-1 in some tumors in vivo, amongst which lung adenocarcinoma, is associated with increased tumor aggressiveness, metastatic potential and suppression of apoptosis. In the present study we investigated the role of Cav-1 in metastatic lung cancer proliferation. Cell lines were from metastatic lesions of lung adenocarcinoma (RAL) and of small cell lung carcinoma (SCLC-R1), in which we found Cav-1 expressed at high levels. Results show that siRNA-mediated down-regulation of Cav-1 caused stable arrest of proliferation in both cell lines. A marked reduction of cyclin D1 and of CDK4 expression was evident in the cells transfected with Cav-1 siRNA and consequently of phospho-Rb on ser(795) and ser(780). Furthermore, a significant decrease of the expression of phosphorylated AICT and of its down-stream effectors phosphorylated ERK and STAT3 was evident. Together, these findings indicate that Cav-1 silencing induces an arrest of human metastatic lung proliferation in vitro by a new inhibitory pathway in lung cancer and provide new insights into the molecular mechanisms underlying the pro-survival and tumor-promoting functions of Cav-1. (c) 201 2 Elsevier Inc. All rights reserved.
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