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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Deletion of XPC leads to lung tumors in mice and is associated with early events in human lung carcinogenesis
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Deletion of XPC leads to lung tumors in mice and is associated with early events in human lung carcinogenesis

机译：XPC的删除导致小鼠肺部肿瘤，并与人类肺癌发生的早期事件有关

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摘要

Chromosome 3p and 1p-deletions are among the most frequent genetic changes in human lung cancer and although candidate tumor suppressor genes have been identified in these regions, no causative correlations have been drawn between deletion or mutation of these and lung carcinogenesis. We identify XPC and Gadd45a as genes within each of these regions involved in lung tumor initiation and progression, respectively. One hundred percent of XPC-/- mice develop multiple spontaneous lung tumors with a minority progressing to non-small cell lung adenocarcinoma, occasionally with metastasis to adjacent lymph nodes. Deletion of Gadd45a alone does not lead to increased lung tumors in mice, but coupled with an XPC deletion, it results in lung tumor progression. Analysis of published data indicated allelic loss of XPC in most human lung tumors and allelic loss of Gadd45a in some human lung and other cancer types. Because DNA repair capacity is compromised in XPC+/- cells, it is possible that the loss of a single XPC allele in the human lung might confer a mutator phenotype. Coupled with cigarette carcinogens, decreased DNA repair would lead to additional mutations in genes such as p53 that are frequent targets in lung cancer.
机译：染色体3p和1p缺失是人类肺癌中最常见的遗传变化之一，尽管在这些区域中已鉴定出候选的抑癌基因，但在这些区域的缺失或突变与肺致癌之间未发现因果关系。我们将XPC和Gadd45a分别识别为涉及肺肿瘤起始和进展的每个区域中的基因。 100％的XPC-/-小鼠发展为多发性自发性肺肿瘤，少数进展为非小细胞肺腺癌，偶而转移至相邻的淋巴结。单独删除Gadd45a不会导致小鼠肺部肿瘤增加，但与XPC缺失相结合，会导致肺部肿瘤进展。已发表数据的分析表明，在大多数人肺肿瘤中XPC等位基因缺失，在某些人肺和其他癌症类型中Gadd45a等位基因缺失。由于XPC +/-细胞中的DNA修复能力受到损害，因此人肺中单个XPC等位基因的缺失可能会赋予突变体表型。再加上香烟致癌物，减少的DNA修复会导致p53等基因的额外突变，而这些突变是肺癌的常见靶标。

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