2024-03-28T22:47:51Zhttp://repisalud.isciii.es/oai/requestoai:repisalud.isciii.es:20.500.12105/66902022-11-02T09:25:51Zcom_20.500.12105_2152com_20.500.12105_2051com_20.500.12105_2144com_20.500.12105_2145col_20.500.12105_2153col_20.500.12105_2146
00925njm 22002777a 4500
dc
Pellinen, Teijo
author
Blom, Sami
author
Sanchez, Sara
author
Valimaki, Katja
author
Mpindi, John-Patrick
author
Azegrouz, Hind
author
Strippoli, Raffaele
author
Nieto-Arellano, Rocio
author
Viton, Mariano
author
Palacios, Irene
author
Turkki, Riku
author
Wang, Yinhai
author
Sanchez-Alvarez, Miguel
author
Nordling, Stig
author
Butzow, Anna
author
Mirtti, Tuomas
author
Rannikko, Antti
author
Montoya, Maria
author
Kallioniemi, Olli
author
del Pozo, Miguel Angel
author
2018
Caveolin-1 (CAV1) is over-expressed in prostate cancer (PCa) and is associated with adverse prognosis, but the molecular mechanisms linking CAV1 expression to disease progression are poorly understood. Extensive gene expression correlation analysis, quantitative multiplex imaging of clinical samples, and analysis of the CAV1-dependent transcriptome, supported that CAV1 re-programmes TGF beta signalling from tumour suppressive to oncogenic (i.e. induction of SLUG, PAI-1 and suppression of CDH1, DSP, CDKN1A). Supporting such a role, CAV1 knockdown led to growth arrest and inhibition of cell invasion in prostate cancer cell lines. Rationalized RNAi screening and high-content microscopy in search for CAV1 upstream regulators revealed integrin beta1 (ITGB1) and integrin associated proteins as CAV1 regulators. Our work suggests TGF beta signalling and beta1 integrins as potential therapeutic targets in PCa over-expressing CAV1, and contributes to better understand the paradoxical dual role of TGF beta in tumour biology.
Sci Rep. 2018; 8(1):2338
2045-2322
http://hdl.handle.net/20.500.12105/6690
29402961
10.1038/s41598-018-20161-2
Scientific Reports
ITGB1-dependent upregulation of Caveolin-1 switches TGF beta signalling from tumour-suppressive to oncogenic in prostate cancer