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首页> 外文期刊>Cancer Cell >Loss of p21 permits carcinogenesis from chronically damaged liver and kidney epithelial cells despite unchecked apoptosis.
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Loss of p21 permits carcinogenesis from chronically damaged liver and kidney epithelial cells despite unchecked apoptosis.

机译：尽管未检查细胞凋亡，p21的丢失仍可从慢性受损的肝和肾上皮细胞中致癌。

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摘要

Accumulation of toxic metabolites in hereditary tyrosinemia type I (HT1) patients leads to chronic DNA damage and the highest risk for hepatocellular carcinomas (HCCs) of any human disease. Here we show that hepatocytes of HT1 mice exhibit a profound cell-cycle arrest that, despite concomitant apoptosis resistance, causes mortality from impaired liver regeneration. However, additional loss of p21 in HT1 mice restores the proliferative capabilities of hepatocytes and renal proximal tubular cells. This growth response compensates cell loss due to uninhibited apoptosis and enables animal survival but rapidly leads to HCCs, renal cysts, and renal carcinomas. Thus, p21's antiproliferative function is indispensable for the suppression of carcinogenesis from chronically injured liver and renal epithelial cells and cannot be compensated by apoptosis.
机译：I型遗传性酪氨酸血症（HT1）患者中有毒代谢产物的积累导致慢性DNA损伤，是任何人类疾病中肝细胞癌（HCC）的最高风险。在这里，我们显示HT1小鼠的肝细胞表现出深远的细胞周期停滞，尽管伴随有凋亡抗性，但会导致肝再生受损而导致死亡。但是，HT1小鼠中p21的额外损失恢复了肝细胞和肾近端肾小管细胞的增殖能力。这种生长反应可以补偿由于不受抑制的细胞凋亡而造成的细胞损失，并使动物得以存活，但会迅速导致肝癌，肾囊肿和肾癌。因此，p21的抗增殖功能对于抑制慢性损伤的肝和肾上皮细胞的癌变是必不可少的，并且不能通过凋亡来补偿。

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