Stopping transformed cancer cell growth by rigidity sensing.
Journal
Nature materials
ISSN: 1476-4660
Titre abrégé: Nat Mater
Pays: England
ID NLM: 101155473
Informations de publication
Date de publication:
02 2020
02 2020
Historique:
received:
29
09
2018
accepted:
11
09
2019
pubmed:
30
10
2019
medline:
24
11
2020
entrez:
30
10
2019
Statut:
ppublish
Résumé
A common feature of cancer cells is the alteration of kinases and biochemical signalling pathways enabling transformed growth on soft matrices, whereas cytoskeletal protein alterations are thought to be a secondary issue. However, we report here that cancer cells from different tissues can be toggled between transformed and rigidity-dependent growth states by the absence or presence of mechanosensory modules, respectively. In various cancer lines from different tissues, cells had over tenfold fewer rigidity-sensing contractions compared with normal cells from the same tissues. Restoring normal levels of cytoskeletal proteins, including tropomyosins, restored rigidity sensing and rigidity-dependent growth. Further depletion of other rigidity sensor proteins, including myosin IIA, restored transformed growth and blocked sensing. In addition, restoration of rigidity sensing to cancer cells inhibited tumour formation and changed expression patterns. Thus, the depletion of rigidity-sensing modules through alterations in cytoskeletal protein levels enables cancer cell growth on soft surfaces, which is an enabling factor for cancer progression.
Identifiants
pubmed: 31659296
doi: 10.1038/s41563-019-0507-0
pii: 10.1038/s41563-019-0507-0
pmc: PMC7477912
mid: NIHMS1625138
doi:
Substances chimiques
Cytoskeletal Proteins
0
TPM3 protein, human
0
Tropomyosin
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
239-250Subventions
Organisme : NIGMS NIH HHS
ID : R01 GM113022
Pays : United States
Commentaires et corrections
Type : CommentIn
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