Research Papers:

Revealing potential molecular targets bridging colitis and colorectal cancer based on multidimensional integration strategy

Xu Guan, Ying Yi, Yan Huang, Yongfei Hu, Xiaobo Li, Xishan Wang, Huihui Fan, Guiyu Wang and Dong Wang _

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Oncotarget. 2015; 6:37600-37612. https://doi.org/10.18632/oncotarget.6067

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Xu Guan1,*, Ying Yi2,*, Yan Huang2,*, Yongfei Hu2, Xiaobo Li3, Xishan Wang1, Huihui Fan2, Guiyu Wang1 and Dong Wang2,4

1 Department of Colorectal Cancer Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, China

2 College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China

3 Department of Pathology, Harbin Medical University, Harbin, China

4 Department of Biochemistry and Molecular Biology, Shantou University Medical College, Shantou, China

* These authors have contributed equally to this work

Correspondence to:

Dong Wang, email:

Guiyu Wang, email:

Huihui Fan, email:

Xishan Wang, email:

Keywords: colorectal cancer, colitis, crosstalk, pivot, network analysis

Received: August 16, 2015 Accepted: September 24, 2015 Published: October 10, 2015


Chronic inflammation may play a vital role in the pathogenesis of inflammation-associated tumors. However, the underlying mechanisms bridging ulcerative colitis (UC) and colorectal cancer (CRC) remain unclear. Here, we integrated multidimensional interaction resources, including gene expression profiling, protein-protein interactions (PPIs), transcriptional and post-transcriptional regulation data, and virus-host interactions, to tentatively explore potential molecular targets that functionally link UC and CRC at a systematic level. In this work, by deciphering the overlapping genes, crosstalking genes and pivotal regulators of both UC- and CRC-associated functional module pairs, we revealed a variety of genes (including FOS and DUSP1, etc.), transcription factors (including SMAD3 and ETS1, etc.) and miRNAs (including miR-155 and miR-196b, etc.) that may have the potential to complete the connections between UC and CRC. Interestingly, further analyses of the virus-host interaction network demonstrated that several virus proteins (including EBNA-LP of EBV and protein E7 of HPV) frequently inter-connected to UC- and CRC-associated module pairs with their validated targets significantly enriched in both modules of the host. Together, our results suggested that multidimensional integration strategy provides a novel approach to discover potential molecular targets that bridge the connections between UC and CRC, which could also be extensively applied to studies on other inflammation-related cancers.

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