Journal
SCIENTIFIC REPORTS
Volume 8, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-018-20161-2
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Funding
- Spanish Ministry of Science and Innovation (MICINN) [SAF2011-25047, CSD2009-0016]
- Spanish Ministry of Economy and Competitiveness (MINECO) [SAF2014-51876-R]
- FEDER funds
- Fundacio La Marato de TV3 [674/C/2013]
- Worldwide Cancer Research Foundation [AICR 15-0404]
- Academy of Finland Center of Excellence in Translational Cancer Biology [251314]
- Sigrid Juselius Foundation
- Cancer Society of Finland
- CNIC Postdoctoral Program
- Academy of Finland [253662]
- Emil Aaltonen foundation
- Wihuri foundations
- Magnus Ehrnrooth foundation
- MINECO
- Pro-CNIC Foundation
- Severo Ochoa Center of Excellence (MINECO) [SEV-2015-0505]
- [BIO2014-62200-EXP]
- Academy of Finland (AKA) [253662, 253662] Funding Source: Academy of Finland (AKA)
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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.
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