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- W4362678212 abstract "Cell remodeling relies on dynamic rearrangements of cell contacts powered by the actin cytoskeleton. The tumor suppressor adenomatous polyposis coli (APC) nucleate actin filaments (F-actin) and localizes at cell junctions. Whether APC-driven actin nucleation acts in cell junction remodeling remains unknown. By combining bioimaging and genetic tools with artificial intelligence algorithms applied to colorectal cancer cell, we found that the APC-dependent actin pool contributes to sustaining levels of F-actin, as well as E-cadherin and occludin protein levels at cell junctions. Moreover, this activity preserved cell junction length and angle, as well as vertex motion and integrity. Loss of this F-actin pool led to larger cells with slow and random cell movement within a sheet. Our findings suggest that APC-driven actin nucleation promotes cell junction integrity and dynamics to facilitate collective cell remodeling and motility. This offers a new perspective to explore the relevance of APC-driven cytoskeletal function in gut morphogenesis." @default.
- W4362678212 created "2023-04-07" @default.
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- W4362678212 date "2023-05-01" @default.
- W4362678212 modified "2023-09-25" @default.
- W4362678212 title "APC-driven actin nucleation powers collective cell dynamics in colorectal cancer cells" @default.
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- W4362678212 doi "https://doi.org/10.1016/j.isci.2023.106583" @default.
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