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Mechanism of cell proliferation--cell cycle, oncogenes, and senescence

机译：细胞增殖的机制-细胞周期，致癌基因和衰老

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Cell proliferation is regulated through a transition between the G0 phase and cell cycle. We isolated a mammalian temperature-sensitive mutant cell line defective in the function from the G0 phase to cell cycle. Senescent human somatic cells fail to enter into the cell cycle from the G0 phase with stimulation by any growth factor. Telomere shortening was found to be a cause of cellular senescence, and reexpression of telomerase immortalized human somatic cells. Immortalized human somatic cells showed normal phenotypes and were useful not only for basic research but also for clinical and applied fields. The importance of p53 and p21 activation/induction i now well accepted in the signal transduction process from telomere shortening to growth arrest, but the precise mechanism is largely unknown as yet. We found that the MAP kinase cascade and histone acetylase have an important role in the signaling process to express p21. Tumor tissues and cells were found to have strong telomerase activity, while most normal somatic human tissues showed very weak or no activity. Telomerase activity was shown to be a good marker for early tumor diagnosis because significant telomerase activity was detected in very early tumors or even in some precancerous tissues compared with adjacent normal tissues. Telomere/telomerase is a candidate target for cancer chemotherapeutics, and an agent that abrogated telomere functions was found to kill tumor cells effectively by inducing apoptosis whereas it showed no effect on the viability of normal cells.
机译：细胞增殖是通过G0期和细胞周期之间的过渡来调节的。我们分离了从G0期到细胞周期在功能上有缺陷的哺乳动物温度敏感突变细胞系。在任何生长因子的刺激下，衰老的人类体细胞都无法从G0期进入细胞周期。发现端粒缩短是细胞衰老的原因，端粒酶永生化人体细胞的重新表达。永生化的人体体细胞表现出正常的表型，不仅可用于基础研究，而且可用于临床和应用领域。从端粒缩短到生长停滞的信号转导过程中，p53和p21激活/诱导的重要性现在已为人们所接受，但确切的机制目前尚不清楚。我们发现，MAP激酶级联反应和组蛋白乙酰化酶在表达p21的信号传导过程中具有重要作用。发现肿瘤组织和细胞具有很强的端粒酶活性，而大多数正常的人体细胞组织则显示非常弱或没有活性。端粒酶活性被证明是早期肿瘤诊断的良好标志物，因为与邻近的正常组织相比，在非常早期的肿瘤甚至某些癌前组织中都检测到了显着的端粒酶活性。端粒/端粒酶是癌症化疗药物的候选靶标，发现端粒功能消失的药物可通过诱导细胞凋亡有效杀死肿瘤细胞，但对正常细胞的存活率没有影响。

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