Ornithine decarboxylase induction during B1 progression of normal and Rous sarcoma virus-transformed cells.
Ornithine decarboxylase induction during B1 progression of normal and Rous sarcoma virus-transformed cells.
复制标题
正常和劳斯肉瘤病毒转化细胞 B1 进展过程中鸟氨酸脱羧酶的诱导。
作者：
M. K. Haddox;B. Magun;D. Russell
比较了 Rat-1 成纤维细胞和 B77 野生型劳斯肉瘤病毒 (RSV) 和热敏突变体 LA24/RSV 转化的 Rat-1 成纤维细胞中细胞周期 G1 期鸟氨酸脱羧酶 (ODC) 的诱导情况。在 Rat-1 细胞中，G1 中期可检测到的最大酶活性在 G1-S 期间下降至基础水平。 ODC 的增加受到放线菌素 D 和放线菌酮的抑制，并且依赖于血清生长因子的添加。 Rat-1（B77野生型RSV）细胞在血清刺激后表达更大量的酶活性，并且在G1中期可检测到的酶活性的最大水平仅下降50％，因此在G1-S过渡期间维持升高的ODC。转化细胞系中酶的增加不依赖于血清生长因子。单独添加新鲜培养基即可诱导酶活性。在存在或不存在血清的情况下进行诱导需要RNA和蛋白质的合成。转化细胞中的 ODC 诱导对外源性腐胺添加的抑制不太敏感。与 Rat-1 细胞相比，需要高 100 倍浓度的二胺才能在 Rat-1（B77 野生型 RSV）中产生相当的抑制作用。发现 ODC 表达特征的这些改变是由热敏病毒突变体 LA24 转化的 Rat-1 细胞系中 RSV 转化功能的结果。为了响应非允许温度（39 度）下的血清刺激，Rat-1（热敏突变体 LA24/RSV）细胞表现出离散的 G1 期 ODC 诱导，而那些维持在允许温度（35 度）的细胞在 G1 和 S 期表现出更大且更长的 ODC 诱导。在不添加任何培养基或血清的情况下从39度到35度的转变刺激了以转化表型方式表达的ODC的诱导。 35 度时比 39 度时需要更高浓度的外源腐胺来抑制 ODC 的诱导。因此，ODC 调节的改变可能是肿瘤表型变化所固有的。
Ornithine decarboxylase (ODC) induction during G1 phase of the cell cycle was compared in Rat-1 fibroblasts and in Rat-1 fibroblasts transformed by the B77 wild-type Rous sarcoma virus (RSV) and by the thermosensitive mutant LA24/RSV. In Rat-1 cells, maximal enzyme activity detectable at mid G1 declined to basal levels by G1-S. The ODC increase was inhibited by actinomycin D and cycloheximide and was dependent on the addition of serum growth factors. Rat-1 (B77 wild-type RSV) cells expressed a greater amount of enzyme activity after serum stimulation, and the maximal level of enzyme activity detectable at mid G1 declined only 50% so that elevated ODC was maintained during G1-S transition. The enzyme increase in the transformed cell line was not dependent on serum growth factors. Fresh medium addition alone induced enzyme activity. Induction in the presence or absence of serum required both RNA and protein synthesis. ODC induction in the transformed cells was less sensitive to repression by exogenous putrescine addition. A 100-fold greater concentration of the diamine was required to produce comparable inhibition in the Rat-1 (B77 wild-type RSV) as compared to the Rat-1 cell. These alterations in the characteristics of ODC expression were found to be a consequence of the transforming function of RSV in the Rat-1 cell line transformed by the thermosensitive viral mutant LA24. In response to serum stimulation at the nonpermissive temperature (39 degrees), Rat-1 (thermosensitive mutant LA24/RSV) cells displayed a discrete G1-phase ODC induction while those cells maintained at the permissive temperature (35 degrees) exhibited a greater and prolonged ODC induction in G1 and S phases. A shift from 39 to 35 degrees in the absence of any medium or serum addition stimulated the induction of ODC expressed in a transformed phenotypic manner. Greater concentrations of exogenous putrescine were required to repress the induction of ODC at 35 than at 39 degrees. Alterations in ODC regulation, therefore, may be inherent to the neoplastic phenotypic change.