Emerging Laminin-332‒Dependent and ‒Independent Roles for Integrin α3 in Protumorigenic Signaling.

J Invest Dermatol

Cell and Developmental Biology, Faculty of Medicine, Center of Human and Molecular Biology (ZHMB), Saarland University, Homburg, Germany; Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), University of Cologne, Cologne, Germany; Center for Molecular Medicine Cologne (CMMC), University of Cologne, Cologne, Germany. Electronic address:

Published: April 2021

The epidermal integrin α3β1 promotes skin tumorigenesis in experimental models; yet, the underlying molecular mechanisms remain mostly unclear. In their article, Ramovs et al. (2020a) identify two spatially separated α3β1-dependent signaling branches fostering skin tumor outgrowth. In basal keratinocytes, α3β1/laminin (LN)-332 drives FAK/Src activation, whereas in suprabasal layers, junctional α3β1 and the tetraspanin CD151 mediate signal transducer and protein kinase B (Akt)‒dependent survival that is independent of LN-332 binding.

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http://dx.doi.org/10.1016/j.jid.2020.08.017DOI Listing

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