Stopping transformed cancer cell growth by rigidity sensing

Bo Yang, Haguy Wolfenson, Vin Yee Chung, Naotaka Nakazawa, Shuaimin Liu, Junqiang Hu, Ruby Yun Ju Huang, Michael P. Sheetz

Research output: Contribution to journalArticlepeer-review

68 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)239-250
Number of pages12
JournalNature Materials
Issue number2
StatePublished - Feb 1 2020

ASJC Scopus subject areas

  • General Chemistry
  • General Materials Science
  • Condensed Matter Physics
  • Mechanics of Materials
  • Mechanical Engineering


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