Format

Send to

Choose Destination
Sci Rep. 2015 Oct 22;5:15340. doi: 10.1038/srep15340.

A functional module-based exploration between inflammation and cancer in esophagus.

Author information

1
College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, Heilongjiang 150086, China.
2
The Fourth Affiliated Hospital, Harbin Medical University, Harbin, Heilongjiang 150001, China.
3
Department of Network Information Center, Harbin Medical University, Harbin, Heilongjiang 150086, China.

Abstract

Inflammation contributing to the underlying progression of diverse human cancers has been generally appreciated, however, explorations into the molecular links between inflammation and cancer in esophagus are still at its early stage. In our study, we presented a functional module-based approach, in combination with multiple data resource (gene expression, protein-protein interactions (PPI), transcriptional and post-transcriptional regulations) to decipher the underlying links. Via mapping differentially expressed disease genes, functional disease modules were identified. As indicated, those common genes and interactions tended to play important roles in linking inflammation and cancer. Based on crosstalk analysis, we demonstrated that, although most disease genes were not shared by both kinds of modules, they might act through participating in the same or similar functions to complete the molecular links. Additionally, we applied pivot analysis to extract significant regulators for per significant crosstalk module pair. As shown, pivot regulators might manipulate vital parts of the module subnetworks, and then work together to bridge inflammation and cancer in esophagus. Collectively, based on our functional module analysis, we demonstrated that shared genes or interactions, significant crosstalk modules, and those significant pivot regulators were served as different functional parts underlying the molecular links between inflammation and cancer in esophagus.

PMID:
26489668
PMCID:
PMC4614801
DOI:
10.1038/srep15340
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center