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Mechanosensitive Piezo Channels in Cancer: Focus on altered Calcium Signaling in Cancer Cells and in Tumor Progression

Department of Cellular, Computational and Integrative Biology (CIBIO), University of Trento, 38123 Povo (Tn), Italy
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Author to whom correspondence should be addressed.
Cancers 2020, 12(7), 1780; https://doi.org/10.3390/cancers12071780
Received: 14 June 2020 / Revised: 1 July 2020 / Accepted: 2 July 2020 / Published: 3 July 2020
(This article belongs to the Special Issue Targeting Calcium Signaling in Cancer Cells)
Mechanotransduction, the translation of mechanical stimuli into biological signals, is a crucial mechanism involved in the function of fundamentally all cell types. In many solid tumors, the malignant transformation is often associated with drastic changes in cell mechanical features. Extracellular matrix stiffness, invasive growth, and cell mobility are just a few hallmarks present in cancer cells that, by inducing mechanical stimuli, create positive feedbacks promoting cancer development. Among the molecular players involved in these pathophysiological processes, the mechanosensitive Ca2+-permeable Piezo channels have emerged as major transducers of mechanical stress into Ca2+ dependent signals. Piezo channels are overexpressed in several cancers, such as in breast, gastric, and bladder, whereas their downregulation has been described in other cancers. Still, the roles of mechanosensitive Piezos in cancer are somewhat puzzling. In this review, we summarize the current knowledge on the pathophysiological roles of these Ca2+-permeable channels, with special emphasis on their functional involvement in different cancer types progression. View Full-Text
Keywords: piezo channels; cancer progression; calcium signaling; mechanotransduction piezo channels; cancer progression; calcium signaling; mechanotransduction
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MDPI and ACS Style

De Felice, D.; Alaimo, A. Mechanosensitive Piezo Channels in Cancer: Focus on altered Calcium Signaling in Cancer Cells and in Tumor Progression. Cancers 2020, 12, 1780.

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