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首页> 外文期刊>Cell cycle >Restoration of G1/S arrest in E1A+c-Ha-ras-transformed cells by Bcl-2 overexpression.
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Restoration of G1/S arrest in E1A+c-Ha-ras-transformed cells by Bcl-2 overexpression.

机译：Bcl-2过表达恢复E1A + c-Ha-ras转化细胞中G1 / S停滞。

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摘要

Here we show that introduction of human bcl-2 gene into E1A+c-Ha-ras-transformed rat embryo fibroblasts, which are highly susceptible to proapoptotic stimuli and fail to be arrested at the G(1)/S boundary following genotoxic stresses, results not only in inhibition of apoptosis, but also in restoration of the G(1)/S arrest. Overexpression of Bcl-2 did not affect proliferation rate and saturation density of E1A+c-Ha-ras transformants. Genotoxic stresses caused prolong G(1)/S arrest in Bcl-2-overexpressing transformants. Remarkably, levels and activities of Cdk2, cyclins E/A, cyclin E-Cdk2 and cyclin A-Cdk2 were unchanged during G(1)/S arrest. Introduction of Bcl-2 into E1A+c-Ha-ras-transformants resulted in accumulation of p21/Waf-1 without inhibiting cyclin-Cdk complexes. In both parental and Bcl-2-overexpressing cells, p21/Waf-1 was coimmunoprecipitated with ERK 1,2 and JNK 1,2, whereas p38 was found in complexes with p21/Waf-1 only in Bcl-2-overexpressing transformants. JNK 1,2 and p38 but not ERK 1,2 were detected in complexes with the exogenous Bcl-2. However, Bcl-2 did not affect phosphorylation of ERK 1,2, JNK 1,2 and p38. G(1)/S arrest induced by adriamycin and serum withdrawal (but not by IR) was accompanied by release of active forms of p38 from complexes with Bcl-2. We suggest that Bcl-2 restores stress-induced G(1)/S arrest without inhibiting cyclin-Cdk2 complexes and MAPK pathways.
机译：在这里，我们显示了将人类bcl-2基因导入E1A + c-Ha-ras转化的大鼠胚胎成纤维细胞中，该细胞高度易受促凋亡刺激，并且在遗传毒性胁迫下未能被阻滞在G（1）/ S边界，结果不仅抑制细胞凋亡，而且还恢复了G（1）/ S逮捕。 Bcl-2的过表达并不影响E1A + c-Ha-ras转化子的增殖速率和饱和密度。遗传毒性应激导致Bcl-2过表达的转化子中的G（1）/ S逮捕延长。值得注意的是，在G（1）/ S逮捕期间，Cdk2，细胞周期蛋白E / A，细胞周期蛋白E-Cdk2和细胞周期蛋白A-Cdk2的水平和活性没有变化。将Bcl-2引入E1A + c-Ha-ras-转化体中导致p21 / Waf-1积累，而不会抑制细胞周期蛋白-Cdk复合物。在亲本和Bcl-2过表达的细胞中，p21 / Waf-1与ERK 1,2和JNK 1,2共免疫沉淀，而p38仅在Bcl-2过表达的转化子中与p21 / Waf-1形成复合体。在与外源性Bcl-2的复合物中检测到JNK 1,2和p38，但未检测到ERK 1,2。但是，Bcl-2不会影响ERK 1,2，JNK 1,2和p38的磷酸化。阿霉素和血清戒断（但不是红外）引起的G（1）/ S停搏伴随着从Bcl-2配合物中释放出活性形式的p38。我们建议Bcl-2恢复压力诱导的G（1）/ S逮捕，而不抑制细胞周期蛋白Cdk2复合物和MAPK途径。

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