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首页> 外文期刊>Cancer Cell >ID1 and ID3 Regulate the Self-Renewal Capacity of Human Colon Cancer-Initiating Cells through p21
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ID1 and ID3 Regulate the Self-Renewal Capacity of Human Colon Cancer-Initiating Cells through p21

机译：ID1和ID3通过p21调节人结肠癌起始细胞的自我更新能力

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摘要

There is increasing evidence that some cancers are hierarchically organized, sustained by a relatively rare population of cancer-initiating cells (C-ICs). Although the capacity to initiate tumors upon serial transplantation is a hallmark of all C-ICs, little is known about the genes that control this process. Here, we establish that ID1 and ID3 function together to govern colon cancer-initiating cell (CC-IC) self-renewal through cell-cycle restriction driven by the cell-cycle inhibitor p21. Regulation of p21 by ID1 and ID3 is a central mechanism preventing the accumulation of excess DNA damage and subsequent functional exhaustion of CC-ICs. Additionally, silencing of ID1 and ID3 increases sensitivity of CC-ICs to the chemotherapeutic agent oxaliplatin, linking tumor initiation function with chemotherapy resistance.
机译：越来越多的证据表明，某些癌症是由相对较少的癌症起始细胞（C-IC）群体所维持的，是按等级组织的。尽管连续移植后引发肿瘤的能力是所有C-IC的标志，但对控制该过程的基因知之甚少。在这里，我们确定ID1和ID3共同发挥作用，通过细胞周期抑制剂p21驱动的细胞周期限制来控制结肠癌起始细胞（CC-IC）的自我更新。 ID1和ID3对p21的调节是防止过量DNA损伤积累和CC-IC功能衰竭的主要机制。此外，ID1和ID3的沉默会增加CC-IC对化疗药物奥沙利铂的敏感性，从而将肿瘤的起始功能与化疗耐药性联系起来。

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