{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Aifuwa I"],"funding":["Johns Hopkins University","NIA NIH HHS","National Institutes of Health","National Institute on Aging","National Science Foundation"],"pagination":["pgac270"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9830950"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["2(1)"],"pubmed_abstract":["The presence of senescent cells within tissues has been functionally linked to malignant transformations. Here, using tension-gauge tethers technology, particle-tracking microrheology, and quantitative microscopy, we demonstrate that senescent-associated secretory phenotype (SASP) derived from senescent fibroblasts impose nuclear lobulations and volume shrinkage on malignant cells, which stems from the loss of RhoA/ROCK/myosin II-based cortical tension. This loss in cytoskeletal tension induces decreased cellular contractility, adhesion, and increased mechanical compliance. These SASP-induced morphological changes are, in part, mediated by Lamin A/C. These findings suggest that SASP induces defective outside-in mechanotransduction from actomyosin fibers in the cytoplasm to the nuclear lami"],"journal":["PNAS nexus"],"pubmed_title":["Senescent stroma induces nuclear deformations in cancer cells via the inhibition of RhoA/ROCK/myosin II-based cytoskeletal tension."],"pmcid":["PMC9830950"],"funding_grant_id":["U01AG060903","P30 AG021334","U01 AG060903","P30AG021334","PHY1430124"],"pubmed_authors":["Philip JM","Valencia AMJ","Perestrelo T","Kim BC","Reddy K","Luperchio TR","Aifuwa I","Kamat P","Starich B","Agrawal A","Tanrioven D","Ha T"],"additional_accession":[]},"is_claimable":false,"name":"Senescent stroma induces nuclear deformations in cancer cells via the inhibition of RhoA/ROCK/myosin II-based cytoskeletal tension.","description":"The presence of senescent cells within tissues has been functionally linked to malignant transformations. Here, using tension-gauge tethers technology, particle-tracking microrheology, and quantitative microscopy, we demonstrate that senescent-associated secretory phenotype (SASP) derived from senescent fibroblasts impose nuclear lobulations and volume shrinkage on malignant cells, which stems from the loss of RhoA/ROCK/myosin II-based cortical tension. This loss in cytoskeletal tension induces decreased cellular contractility, adhesion, and increased mechanical compliance. These SASP-induced morphological changes are, in part, mediated by Lamin A/C. These findings suggest that SASP induces defective outside-in mechanotransduction from actomyosin fibers in the cytoplasm to the nuclear lami","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2026-03-17T16:03:59.272Z","creation":"2025-04-06T18:02:49.738Z"},"accession":"S-EPMC9830950","cross_references":{"pubmed":["36712940"],"doi":["10.1093/pnasnexus/pgac270"]}}