title: Functional comparison between genes dysregulated in ulcerative colitis and colorectal carcinoma.
abstract: BACKGROUND
  Patients with ulcerative colitis (UC) are predisposed to colitis-associated colorectal cancer (CAC). However, the transcriptional mechanism of the transformation from UC to CAC is not fully understood.
  
  
  METHODS
  Firstly, we showed that CAC and non-UC-associated CRC were very similar in gene expression. Secondly, based on multiple datasets for UC and CRC, we extracted differentially expressed (DE) genes in UC and CRC versus normal controls, respectively. Thirdly, we compared the dysregulation directions (upregulation or downregulation) between DE genes of UC and CRC in CRC-related functions overrepresented with the DE genes of CRC, and proposed a regulatory model to explain the CRC-like dysregulation of genes in UC. A case study for "positive regulation of immune system process" was done to reveal the functional implication of DE genes with reversal dysregulations in these two diseases.
  
  
  RESULTS
  In all the 44 detected CRC-related functions except for "viral transcription", the dysregulation directions of DE genes in UC were significantly similar with their counterparts in CRC, and such CRC-like dysregulation in UC could be regulated by transcription factors affected by pro-inflammatory stimuli for colitis. A small portion of genes in each CRC-related function were dysregulated in opposite directions in the two diseases. The case study showed that genes related to humoral immunity specifically expressed in B cells tended to be upregulated in UC but downregulated in CRC.
  
  
  CONCLUSIONS
  The CRC-like dysregulation of genes in CRC-related functions in UC patients provides hints for understanding the transcriptional basis for UC to CRC transition. A small portion of genes with distinct dysregulation directions in each of the CRC-related functions in the two diseases implicate that their reversal dysregulations might be critical for UC to CRC transition. The cases study indicates that the humoral immune response might be inhibited during the transformation from UC to CRC.
authors.affiliation: College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
authors.forename: Wenyuan
authors.initials: W
authors.lastname: Zhao
authors.forename: Lishuang
authors.initials: L
authors.lastname: Qi
authors.forename: Yao
authors.initials: Y
authors.lastname: Qin
authors.forename: Hongwei
authors.initials: H
authors.lastname: Wang
authors.forename: Beibei
authors.initials: B
authors.lastname: Chen
authors.forename: Ruiping
authors.initials: R
authors.lastname: Wang
authors.forename: Yunyan
authors.initials: Y
authors.lastname: Gu
authors.forename: Chunyang
authors.initials: C
authors.lastname: Liu
authors.forename: Chenguang
authors.initials: C
authors.lastname: Wang
authors.forename: Zheng
authors.initials: Z
authors.lastname: Guo
mesh_terms: D002471:Cell Transformation, Neoplastic / Q000235:genetics* / Q000276:immunology; D003093:Colitis, Ulcerative / Q000235:genetics* / Q000276:immunology; D015179:Colorectal Neoplasms / Q000235:genetics* / Q000276:immunology; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000276:immunology; D053263:Gene Regulatory Networks / Q000276:immunology; D006801:Humans; D007107:Immune System / Q000378:metabolism; D008957:Models, Genetic; D020411:Oligonucleotide Array Sequence Analysis