Bechade C, Calothy G
Institut Curie-Biologie, Centre Universitaire, Orsay, France.
Oncogene. 1991 Dec;6(12):2311-7.
We previously reported that avian retroviruses carrying the v-myc oncogene alone fail to induce sustained proliferation and transformation of non-dividing chicken neuroretina (CNR) cells from 7-day-old embryos. However, v-myc is capable of transforming CNR cells which have been induced to multiply by the v-mil oncogene. These results suggest that entry into the cell cycle is required for the transformation of CNR cells by v-myc. To further assess the role of cell division, we investigated the transforming properties of v-myc in CNR cells conditionally induced to divide by the v-src gene or by modified culture conditions. We show that v-myc transforms CNR cells infected with Rous sarcoma virus mutants which induce cell proliferation in the absence of transformation. Expression of these transforming properties in CNR cells infected with temperature-sensitive v-src mutants depends on the continuous mitogenic activity of p60v-src. We also report that v-myc is able to transform CNR cells and to increase their growth potential under culture conditions which allow transient multiplication of uninfected cells. However, these v-myc-transformed cells rapidly cease to divide when returned to culture conditions that restrict the growth of normal cells. Taken together, these results indicate that transformation of CNR cells by the v-myc oncogene continuously depends on their ability to enter the cell cycle.
我们先前报道,仅携带v-myc癌基因的禽逆转录病毒无法诱导7日龄胚胎的非分裂鸡神经视网膜(CNR)细胞持续增殖和转化。然而,v-myc能够转化已被v-mil癌基因诱导增殖的CNR细胞。这些结果表明,v-myc转化CNR细胞需要进入细胞周期。为了进一步评估细胞分裂的作用,我们研究了v-myc在通过v-src基因或改良培养条件被条件性诱导分裂的CNR细胞中的转化特性。我们发现,v-myc可转化感染了劳氏肉瘤病毒突变体的CNR细胞,这些突变体在不发生转化的情况下诱导细胞增殖。在感染温度敏感型v-src突变体的CNR细胞中,这些转化特性的表达取决于p60v-src持续的促有丝分裂活性。我们还报道,在允许未感染细胞短暂增殖的培养条件下,v-myc能够转化CNR细胞并增加其生长潜力。然而,当这些v-myc转化的细胞回到限制正常细胞生长的培养条件时,它们会迅速停止分裂。综上所述,这些结果表明,v-myc癌基因对CNR细胞的转化持续依赖于它们进入细胞周期的能力。