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Systematic Identification of Core Transcription Factors Mediating Dysregulated Links Bridging Inflammatory Bowel Diseases and Colorectal Cancer

Accumulating evidence shows a tight link between inflammation and cancer. However, comprehensive identification of pivotal transcription factors (i.e., core TFs) mediating the dysregulated links remains challenging, mainly due to a lack of samples that can effectively reflect the connections between...

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Detalles Bibliográficos
Autores principales: Xiao, Yun, Fan, Huihui, Zhang, Yunpeng, Xing, Wenjing, Ping, Yanyan, Zhao, Hongying, Xu, Chaohan, Li, Yiqun, Wang, Li, Li, Feng, Hu, Jing, Huang, Teng, Lv, Yanling, Ren, Huan, Li, Xia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3873387/
https://www.ncbi.nlm.nih.gov/pubmed/24386215
http://dx.doi.org/10.1371/journal.pone.0083495
Descripción
Sumario:Accumulating evidence shows a tight link between inflammation and cancer. However, comprehensive identification of pivotal transcription factors (i.e., core TFs) mediating the dysregulated links remains challenging, mainly due to a lack of samples that can effectively reflect the connections between inflammation and tumorigenesis. Here, we constructed a series of TF-mediated regulatory networks from a large compendium of expression profiling of normal colonic tissues, inflammatory bowel diseases (IBDs) and colorectal cancer (CRC), which contains 1201 samples in total, and then proposed a network-based approach to characterize potential links bridging inflammation and cancer. For this purpose, we computed significantly dysregulated relationships between inflammation and their linked cancer networks, and then 24 core TFs with their dysregulated genes were identified. Collectively, our approach provides us with quite important insight into inflammation-associated tumorigenesis in colorectal cancer, which could also be applied to identify functionally dysregulated relationships mediating the links between other different disease phenotypes.