4.5 Article

Establishment of optimal regulatory network of colorectal cancer based on p42.3 protein

Journal

SAUDI JOURNAL OF BIOLOGICAL SCIENCES
Volume 24, Issue 8, Pages 1781-1786

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.sjbs.2017.11.012

Keywords

p42.3; Colorectal cancer; Gene markers; Protein similarity algorithm; Bayesian theory

Categories

Funding

  1. Natural Science Foundation of Henan Province [162300410290]
  2. National Key R&D Program of China [2016YFC1303200]

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Objective: to establish regulatory network of colorectal cancer involving p42.3 protein and to provide theoretical evidence for deep functional exploration of p42.3 protein in the onset and development of colorectal cancer. Methods: with protein similarity algorithm, reference protein set of p42.3 cell apoptosis was built according to structural features of p42.3. GO and KEGG databases were used to establish regulatory network of tumor cell apoptosis involving p42.3; meanwhile, the largest possible working pathway that involves p42.3 protein was screened out based on Bayesian network theory. Besides, GO and KEGG were used to build regulatory network on early diagnosis gene markers for colorectal cancer including WWOX, K-ras, COX-2, p53, APC, DCC and PTEN, at the same time, a regulatory network of colorectal cancer cell apoptosis which involves p42.3 was established. Results: cell apoptotic regulatory network that p42.3 participates in primarily consists of Bcl-2 family genes and the largest possible pathway is p42.3 -> FKBP -> Bcl-2 centered as FKBP protein. Combined with colorectal cancer regulatory network that involves early diagnosis gene markers, it can be predicted that p42.3 is most likely to regulate the colorectal cancer cell apoptosis through FKBP -> Bcl-2 -> Bax -> caspase-9 -> caspase-3 pathway. Conclusion: the colorectal cancer apoptosis network based on p42.3 established in the study provides theoretical evidence for deep exploration of p42.3 regulatory mechanism and molecular targeting treatment of colorectal cancer. (C) 2017 Production and hosting by Elsevier B.V.on behalf of King Saud University.

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