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dc.contributor.authorLinthicum, W.
dc.contributor.authorThanh, M.-T.H.
dc.contributor.authorVitolo, M.I.
dc.date.accessioned2019-04-29T19:01:00Z
dc.date.available2019-04-29T19:01:00Z
dc.date.issued2018
dc.identifier.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85047907998&doi=10.3390%2fijms19061613&partnerID=40&md5=95ad1e5b9a644e9b01558d5140d006c5
dc.identifier.urihttp://hdl.handle.net/10713/8938
dc.description.abstractIt has previously been shown that the simultaneous activation of PI3K (phosphatidylinositol 3-kinase) and Ras/MAPK (mitogen-activated protein kinases) pathways facilitate tumor growth despite only inducing cancer cell dormancy individually. Determining the impacts on cellular mechanics each pathway incites alone and in unison is critical to developing non-toxic cancer therapies for triple-negative breast cancers. PTEN (phosphatase and tensin homolog) knockout and activated KRAS (Kristen rat sarcoma viral oncogene homolog) overexpression in healthy MCF-10A human breast epithelial cells activated the PI3K and Ras/MAPK pathways, respectively. Cell stiffness and fluidity were simultaneously measured using atomic force microscopy. Results suggest that PTEN knockout reduced cell stiffness and increased cell fluidity independent of PI3K activation. Effects of activated KRAS overexpression on cell stiffness depends on rigidity of cell culture substrate. Activated KRAS overexpression also counteracts the effects of PTEN knockout. Copyright 2018 by the authors. Licensee MDPI, Basel, Switzerland.en_US
dc.description.sponsorshipAcknowledgments: This research is supported by NSF grant CBET-1403257 (Q.W.), IGERT-DGE-1144804 (W.L.), NIH grant K01-CA166576 (M.I.V.), and 122229-IRG-97-153-10-IRG from the American Cancer Society (M.I.V.).en_US
dc.description.urihttps://dx.doi.org/10.3390/ijms19061613en_US
dc.language.isoen_USen_US
dc.publisherMDPI AGen_US
dc.relation.ispartofInternational Journal of Molecular Sciences
dc.subjectAtomic force microscopyen_US
dc.subjectCanceren_US
dc.subjectCell mechanicsen_US
dc.titleEffects of PTEN loss and activated KRAS overexpression on mechanical properties of breast epithelial cellsen_US
dc.typeArticleen_US
dc.identifier.doi10.3390/ijms19061613
dc.identifier.pmid29848992


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