Open AccessPotentiation of growth factor activity by exogenous c-myc expression.
Author(s) -
Vincenzo Sorrentino,
Vladimir Drozdoff,
Martin D. McKinney,
L. Zeitz,
Erwin Fleissner
Publication year - 1986
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.83.21.8167
Subject(s) - platelet derived growth factor receptor , growth factor , biology , microbiology and biotechnology , platelet derived growth factor , cancer research , cell cycle , cell growth , long term potentiation , proto oncogene proteins c myc , gene expression , gene , genetics , receptor
The c-myc oncogene has been implicated in deregulation of cell growth in neoplastic cells and response to "competence-inducing" growth factors in normal cells. In the latter case, expression of c-myc has been shown to be associated with the transition from the G0 to the G1 phase of the cell cycle induced by platelet-derived growth factor (PDGF). In the work reported here, we have introduced the c-myc coding region, in a retroviral vector, into mouse and rat cells. We show that under conditions of anchorage-independent growth, constitutive c-myc expression increases the response of rodent cells to PDGF, as well as to other growth factors of both the competence-inducing and "progression" classes. These effects of the myc product are observed whether or not an exogenous ras gene has also been introduced into the same cells. Possible models for the influence of myc on growth responses are discussed.