生物
杂合子丢失
癌症研究
抑癌基因
肿瘤进展
血管生成
癌变
癌症
表型
血管生成抑制剂
分子生物学
基因
遗传学
等位基因
作者
Rifat Hasina,Andrea Pontier,Mary Jo Fekete,Lee Martin,Xiaoping Qi,Christophe Brigaudeau,Rocky Pramanik,Edith I. Cline,Lionel Coignet,Mark W. Lingen
出处
期刊:Oncogene
[Springer Nature]
日期:2005-10-03
卷期号:25 (4): 588-598
被引量:33
标识
DOI:10.1038/sj.onc.1209070
摘要
Cervical cancer is associated with human papilloma virus infection. However, this infection is insufficient to induce transformation and progression. Loss of heterozygosity analyses suggest the presence of a tumor suppressor gene (TSG) on chromosome 6p21.3-p25. Here we report the cloning NOL7, its mapping to chromosome band 6p23, and localization of the protein to the nucleolus. Fluorescence in situ hybridization analysis demonstrated an allelic loss of an NOL7 in cultured tumor cells and human tumor samples. Transfection of NOL7 into cervical carcinoma cells inhibited their growth in mouse xenografts, confirming its in vivo tumor suppressor activity. The induction of tumor dormancy correlated with an angiogenic switch caused by a decreased production of vascular endothelial growth factor and an increase in the production of the angiogenesis inhibitor thrombospondin-1. These data suggest that NOL7 may function as a TSG in part by modulating the expression of the angiogenic phenotype.
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