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首页> 外文期刊>Cancer Cell >Loss of p53 in Enterocytes Generates an Inflammatory Microenvironment Enabling Invasion and Lymph Node Metastasis of Carcinogen-Induced Colorectal Tumors
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Loss of p53 in Enterocytes Generates an Inflammatory Microenvironment Enabling Invasion and Lymph Node Metastasis of Carcinogen-Induced Colorectal Tumors

机译：肠上皮细胞中p53的丢失产生炎性微环境，使致癌物诱导的大肠肿瘤浸润和淋巴结转移。

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Loss of p53 is considered to allow progression of colorectal tumors from the adenoma to the carcinoma stage. Using mice with an intestinal epithelial cell (IEC)-specific p53 deletion, we demonstrate that loss of p53 alone is insufficient to initiate intestinal tumorigenesis but markedly enhances carcinogen-induced tumor incidence and leads to invasive cancer and lymph node metastasis. Whereas p53 controls DNA damage and IEC survival during the initiation stage, loss of p53 during tumor progression is associated with increased intestinal permeability, causing formation of an NF-κB-dependent inflammatory microenvironment and the induction of epithelial-mesenchymal transition. Thus, we propose a p53-controlled tumor-suppressive function that is independent of its well-established role in cell-cycle regulation, apoptosis, and senescence.
机译：p53的丢失被认为可使大肠肿瘤从腺瘤发展到癌期。使用具有肠上皮细胞（IEC）特异性p53缺失的小鼠，我们证明仅p53的缺失不足以启动肠道肿瘤发生，但显着增强致癌物诱导的肿瘤发生率，并导致浸润性癌症和淋巴结转移。尽管p53控制起始阶段的DNA损伤和IEC存活，但p53在肿瘤进展过程中的丧失与肠道通透性增加相关，导致形成NF-κB依赖性炎性微环境并诱导上皮-间质转化。因此，我们提出了p53控制的肿瘤抑制功能，其独立于其在细胞周期调节，细胞凋亡和衰老中的既定作用。

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