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                  <mods:dateIssued encoding="iso8601">2020-06</mods:dateIssued>
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               <mods:identifier type="citation">Cancer Metastasis Rev. 2020; 39:485–503</mods:identifier>
               <mods:identifier type="doi">10.1007/s10555-020-09900-y</mods:identifier>
               <mods:identifier type="e-issn">1573-7233</mods:identifier>
               <mods:identifier type="journal">Cancer metastasis reviews</mods:identifier>
               <mods:identifier type="pubmedID">32514892</mods:identifier>
               <mods:identifier type="uri">http://hdl.handle.net/20.500.12105/10702</mods:identifier>
               <mods:abstract>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.</mods:abstract>
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                  <mods:title>Tumor-stroma biomechanical crosstalk: a perspective on the role of caveolin-1 in tumor progression.</mods:title>
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