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dc.contributor.authorWang, Hong-Bei
dc.contributor.authorDembo, Micah
dc.contributor.authorWang, Yu-Li
dc.date2022-08-11T08:09:31.000
dc.date.accessioned2022-08-23T16:34:18Z
dc.date.available2022-08-23T16:34:18Z
dc.date.issued2000-10-13
dc.date.submitted2007-12-21
dc.identifier.citation<p>Am J Physiol Cell Physiol. 2000 Nov;279(5):C1345-50.</p>
dc.identifier.issn0363-6143 (Print)
dc.identifier.doi10.1152/ajpcell.2000.279.5.C1345
dc.identifier.pmid11029281
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38299
dc.description.abstractOne of the hallmarks of oncogenic transformation is anchorage-independent growth (27). Here we demonstrate that responses to substrate rigidity play a major role in distinguishing the growth behavior of normal cells from that of transformed cells. We cultured normal or H-ras-transformed NIH 3T3 cells on flexible collagen-coated polyacrylamide substrates with similar chemical properties but different rigidity. Compared with cells cultured on stiff substrates, nontransformed cells on flexible substrates showed a decrease in the rate of DNA synthesis and an increase in the rate of apoptosis. These responses on flexible substrates are coupled to decreases in cell spreading area and traction forces. In contrast, transformed cells maintained their growth and apoptotic characteristics regardless of substrate flexibility. The responses in cell spreading area and traction forces to substrate flexibility were similarly diminished. Our results suggest that normal cells are capable of probing substrate rigidity and that proper mechanical feedback is required for regulating cell shape, cell growth, and survival. The loss of this response can explain the unregulated growth of transformed cells.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11029281&dopt=Abstract ">Link to article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1152/ajpcell.2000.279.5.C1345
dc.subject3T3 Cells
dc.subjectAnimals
dc.subjectApoptosis
dc.subjectCell Division
dc.subjectCell Line, Transformed
dc.subjectDNA
dc.subjectMice
dc.subjectReference Values
dc.subjectSubstrate Specificity
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleSubstrate flexibility regulates growth and apoptosis of normal but not transformed cells
dc.typeJournal Article
dc.source.journaltitleAmerican journal of physiology. Cell physiology
dc.source.volume279
dc.source.issue5
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/117
dc.identifier.contextkey407412
html.description.abstract<p>One of the hallmarks of oncogenic transformation is anchorage-independent growth (27). Here we demonstrate that responses to substrate rigidity play a major role in distinguishing the growth behavior of normal cells from that of transformed cells. We cultured normal or H-ras-transformed NIH 3T3 cells on flexible collagen-coated polyacrylamide substrates with similar chemical properties but different rigidity. Compared with cells cultured on stiff substrates, nontransformed cells on flexible substrates showed a decrease in the rate of DNA synthesis and an increase in the rate of apoptosis. These responses on flexible substrates are coupled to decreases in cell spreading area and traction forces. In contrast, transformed cells maintained their growth and apoptotic characteristics regardless of substrate flexibility. The responses in cell spreading area and traction forces to substrate flexibility were similarly diminished. Our results suggest that normal cells are capable of probing substrate rigidity and that proper mechanical feedback is required for regulating cell shape, cell growth, and survival. The loss of this response can explain the unregulated growth of transformed cells.</p>
dc.identifier.submissionpathoapubs/117
dc.contributor.departmentDepartment of Physiology
dc.source.pagesC1345-50


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