基础医学与临床 ›› 2016, Vol. 36 ›› Issue (10): 1437-1440.
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张记1,吴玉章2,阎萍3
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摘要： 染色质重塑复合体SWI/SNF亚基基因在肿瘤中突变率高达约20%，突变造成编码蛋白失活及整个复合体功能异常，导致肿瘤发生。目前SWI/SNF抑制肿瘤的已知机制主要包括其与Polycomb复合体间的表观拮抗及与c-Myc及PIK3CA等致癌基因信号通路协同作用等。
关键词: 关键词: SWI/SNF, 染色质重塑, ARID1A
Abstract: The mutations of SWI/SNF subunits genes, with about 20% high in human cancers, promote oncogenesis by inactivating the function of encoding proteins and further perturbing the whole function of SWI/SNF complexes. The main yet known mechanisms by which SWI/SNF suppress tumor development include its epigenetic antagonism with Polycomb complexes, as well as synergetic interaction with other oncogene signaling such as c-Myc and PIK3CA.
Key words: Key words: SWI/SNF, chromatin remodeling, ARID1A
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R730.2
张记 吴玉章 阎萍. SWI/SNF染色质重塑在肿瘤中的研究进展[J]. 基础医学与临床, 2016, 36(10): 1437-1440.
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http://journal11.magtechjournal.com/Jwk_jcyxylc/CN/Y2016/V36/I10/1437
