Sorrentino V, Drozdoff V, McKinney M D, Zeitz L, Fleissner E
Proc Natl Acad Sci U S A. 1986 Nov;83(21):8167-71. doi: 10.1073/pnas.83.21.8167.
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.
c-myc癌基因与肿瘤细胞中细胞生长的失调以及正常细胞对“诱导能力”生长因子的反应有关。在后一种情况下，已表明c-myc的表达与血小板衍生生长因子（PDGF）诱导的细胞周期从G0期向G1期的转变相关。在本文报道的研究中，我们将逆转录病毒载体中的c-myc编码区导入小鼠和大鼠细胞。我们发现，在不依赖贴壁生长的条件下，组成型c-myc表达增强了啮齿动物细胞对PDGF以及对诱导能力和“进展”类别的其他生长因子的反应。无论是否将外源性ras基因也导入同一细胞，都能观察到myc产物的这些作用。文中讨论了myc对生长反应影响的可能模型。
