Gu Jia, Li TongJuan, Zhao Lei, Liang Xue, Fu Xing, Wang Jue, Shang Zhen, Huang Wei, Zhou Jianfeng
Department of Hematology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
Biomed Res Int. 2017;2017:5326370. doi: 10.1155/2017/5326370. Epub 2017 Feb 21.
PAX5 encodes a transcription factor essential for B-cell differentiation, and PAX5 haploinsufficiency is involved in tumorigenesis. There were few studies on how PAX5 haploinsufficiency regulated genes expression to promote tumorigenesis. In this study, we constructed the cell model of PAX5 haploinsufficiency using gene editing technology in Raji cells, detected differentially expressed genes in PAX5 haploinsufficiency Raji cells, and used protein-protein interaction networks and cluster analysis to comprehensively investigate the cellular pathways involved in PAX5 haploinsufficiency. The clusters of gene transcription, inflammatory and immune response, and cancer pathways were identified as three important pathways associated with PAX5 haploinsufficiency in Raji cells. These changes hinted that the mechanism of PAX5 haploinsufficiency promoting tumorigenesis may be related to genomic instability, immune tolerance, and tumor pathways.
PAX5编码一种对B细胞分化至关重要的转录因子，PAX5单倍体不足参与肿瘤发生。关于PAX5单倍体不足如何调节基因表达以促进肿瘤发生的研究很少。在本研究中，我们利用基因编辑技术在Raji细胞中构建了PAX5单倍体不足的细胞模型，检测了PAX5单倍体不足的Raji细胞中的差异表达基因，并使用蛋白质-蛋白质相互作用网络和聚类分析来全面研究PAX5单倍体不足所涉及的细胞途径。基因转录、炎症和免疫反应以及癌症途径的聚类被确定为与Raji细胞中PAX5单倍体不足相关的三个重要途径。这些变化提示PAX5单倍体不足促进肿瘤发生的机制可能与基因组不稳定、免疫耐受和肿瘤途径有关。
