Adseverin modulates morphology and invasive function of MCF7 cells.

Autor: Tanic J; Faculty of Dentistry, University of Toronto, Canada., Wang Y; Faculty of Dentistry, University of Toronto, Canada., Lee W; Faculty of Dentistry, University of Toronto, Canada., Coelho NM; Faculty of Dentistry, University of Toronto, Canada., Glogauer M; Faculty of Dentistry, University of Toronto, Canada., McCulloch CA; Faculty of Dentistry, University of Toronto, Canada. Electronic address: christopher.mcculloch@utoronto.ca.
Jazyk: angličtina
Zdroj: Biochimica et biophysica acta. Molecular basis of disease [Biochim Biophys Acta Mol Basis Dis] 2019 Oct 01; Vol. 1865 (10), pp. 2716-2725. Date of Electronic Publication: 2019 Jul 29.
DOI: 10.1016/j.bbadis.2019.07.015
Abstrakt: Adseverin (Ads) is a Ca 2+ -dependent actin-capping and severing protein that is highly expressed in gastric, prostate and bladder cancer cells. Currently it is unknown whether Ads contributes to the subcortical actin remodeling associated with the formation of cell extensions and matrix invasion in cancer. We compared cell extension formation and matrix degradation in Ads wildtype and Ads-null MCF7 breast cancer cells generated by CRISPR/Cas9. Compared with wildtype, Ads-null cells plated on fibronectin or collagen exhibited a more circular morphology with shorter cell extensions (37% reduction on fibronectin; p < 0.001). Reconstitution of Ads in Ads-null cells restored the formation of cell extensions (p < 0.05). While cell migration on two-dimensional matrices was unchanged by Ads deletion, the formation of cell extensions across Transwell membranes was reduced (~40% reduction, p < 0.05). When plated on fibrillar collagen, compared with wildtype, Ads-null cells showed reduced expression of MT1-MMP, collagen degradation (p < 0.05) and phagocytosis of collagen-coated beads (25% reduction; p = 0.001). We conclude that Ads is involved in the formation of cell extensions and collagen degradation in MCF7 cells, which may in turn affect matrix invasion and metastasis.
(Copyright © 2019 The Authors. Published by Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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