Journal
CANCER AND METASTASIS REVIEWS
Volume 39, Issue 2, Pages 485-503Publisher
SPRINGER
DOI: 10.1007/s10555-020-09900-y
Keywords
Mechanobiology; Caveolae; Caveolin-1; Cancer; Stromal remodeling; Extracellular matrix (ECM); Cancer-associated fibroblasts (CAFs); YAP; TAZ; Integrin signaling; Cell contraction; Tumor cell reprogramming; Metastasis
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Funding
- Spanish Ministry of Economy, Industry and Competitiveness (MINECO) [SAF2011-25047, SAF2014-51876-R, SAF2017-83130-R, MINSEV1512-07-2016, CSD2009-0016, BFU2016-81912-REDC]
- Worldwide Cancer Research Foundation [15-0404]
- Comunidad Autonoma de Madrid/FEDER, Spain [P2018/NMT4443]
- Fundacio LaMarato de TV3 [674/C/2013, 201936]
- European Union Horizon 2020 research and innovation programme under Marie Sklodowska-Curie grant [641639]
- CNIC IPP fellowship (COFUND programme 2014)
- Instituto de Salud Carlos III (ISCIII), the Ministerio de Ciencia, Innovacion y Universidades (MCNU)
- Pro CNIC Foundation
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Tumor stiffening is a hallmark of malignancy that actively drives tumor progression and aggressiveness. Recent research has shed light onto several molecular underpinnings of this biomechanical process, which has a reciprocal crosstalk between tumor cells, stromal fibroblasts, and extracellular matrix remodeling at its core. This dynamic communication shapes the tumor microenvironment; significantly determines disease features including therapeutic resistance, relapse, or metastasis; and potentially holds the key for novel antitumor strategies. Caveolae and their components emerge as integrators of different aspects of cell function, mechanotransduction, and ECM-cell interaction. Here, we review our current knowledge on the several pivotal roles of the essential caveolar component caveolin-1 in this multidirectional biomechanical crosstalk and highlight standing questions in the field.
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