# A Network‐Based Association of IBD and Colorectal Cancer Using Proteomics Data

## TL;DR

This study explores shared molecular mechanisms between inflammatory bowel disease and colorectal cancer using proteomics data to identify key proteins and pathways.

## Contribution

The study introduces a multi-omics network approach to uncover shared molecular links between IBD and CRC.

## Key findings

- Seven CRC-associated proteins were significantly upregulated in CRC, with six also elevated in IBD.
- AHCY and LCN2 were identified as central hubs linking inflammatory and metabolic pathways.
- NF-κB and GATA2 emerged as key transcriptional regulators confirmed in CRC tissues.

## Abstract

Colorectal cancer (CRC) is a major cause of morbidity and mortality, with chronic inflammation from inflammatory bowel disease (IBD) representing a well‐established risk factor. Clarifying shared molecular mechanisms may facilitate early detection and prevention strategies.

Proteomic data from the UK Biobank were analysed using the Olink proximity extension assay for seven CRC‐associated proteins (TFF3, TFF1, AHCY, RETN, LCN2, SELE and CEACAM5) previously identified via machine learning. Expression levels in CRC and IBD cases were compared with controls. Multilayer interaction networks, incorporating protein–protein, protein–metabolite and transcription factor–protein interactions, were generated using OmicsNet. Findings were validated in the Colonomics transcriptomic dataset.

All seven proteins were significantly upregulated in CRC; six (excluding CEACAM5) were also elevated in IBD. Network analysis identified AHCY and LCN2 as central hubs linking inflammatory and metabolic pathways. NF‐κB and GATA2 emerged as recurrent transcriptional regulators. Colonomics validation confirmed upregulation of AHCY, LCN2 and SELE in CRC tissues.

This multi‐omics network analysis reveals a shared molecular framework between IBD and CRC, with inflammation as a key driver of colorectal carcinogenesis.