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• W2130026994 abstract "Anchorage-independent growth is a hallmark of transformed cells, but little is known of the molecular mechanisms that underlie this phenomenon. We describe here studies of cell cycle control of anchorage-independent growth induced by the ras oncogene, with the use of a somatic cell mutant fibroblast line (ER-1-2) that is specifically defective in oncogene-mediated, anchorage-independent growth. Control, nontransformed PKC3-F4 cells and ER-1-2 cells cannot proliferate in semisolid medium. Three important cell cycle events are dependent on adhesion of these cells to a substratum: phosphorylation of the retinoblastoma protein, pRB; cyclin E-dependent kinase activity; and cyclin A expression. PKC3-F4 cells that express ras (PKC3-F4/ras cells) proliferate in nonadherent cultures, and each of these three events occurs in the absence of adhesion in PKC3-F4/ras cells. Thus, ras can override the adhesion requirement of cellular functions that are necessary for cell cycle progression. ER-1-2 cells that express ras (ER-1-2/ras cells) possess hyperphosphorylated forms of pRB and cyclin E-dependent kinase activity in the absence of adhesion but remain adhesion dependent for expression of cyclin A. The adhesion dependence of pRB phosphorylation and cyclin E-dependent kinase activity is therefore dissociable from the adhesion dependence of cyclin A expression. Furthermore, ectopic expression of cyclin A is sufficient to rescue anchorage-independent growth of ER-1-2/ras cells but does not induce anchorage-independent growth of PKC3-F4 or ER-1-2 cells. However, like pRB phosphorylation and cyclin E-dependent kinase activity, the kinase activity associated with ectopically expressed cyclin A is dependent on cell adhesion, and this dependence is overcome by ras. Thus, the induction of anchorage-independent growth by ras may involve multiple signals that lead to both expression of cyclin A and activation of G1 cyclin-dependent kinase activities in the absence of cell adhesion." @default.
• W2130026994 created "2016-06-24" @default.
• W2130026994 creator A5053589398 @default.
• W2130026994 creator A5055732430 @default.
• W2130026994 date "1996-07-01" @default.
• W2130026994 modified "2023-10-11" @default.
• W2130026994 title "Ras Induces Anchorage-Independent Growth by Subverting Multiple Adhesion-Regulated Cell Cycle Events" @default.
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• W2130026994 doi "https://doi.org/10.1128/mcb.16.7.3370" @default.
• W2130026994 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/231331" @default.
• W2130026994 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/8668152" @default.
• W2130026994 hasPublicationYear "1996" @default.
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