Effects of PTEN loss and activated KRAS overexpression on mechanical properties of breast epithelial cells
JournalInternational Journal of Molecular Sciences
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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.
SponsorsAcknowledgments: 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.).
Identifier to cite or link to this itemhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85047907998&doi=10.3390%2fijms19061613&partnerID=40&md5=95ad1e5b9a644e9b01558d5140d006c5; http://hdl.handle.net/10713/8938