Simple Summary
This study explores how microinflammation—a subtle, long-lasting form of inflammation—connects common metabolic conditions like obesity, type 2 diabetes, and irritable bowel syndrome with cancers of the colon, kidney, and pancreas. By analyzing gene activity across multiple datasets, the research found shared disruptions in how cells process genetic information and manage proteins. Key genes and small regulatory molecules appear to drive these changes and sustain chronic inflammation. These findings suggest that many chronic diseases are linked by the same underlying biological processes. Understanding these connections may support earlier diagnosis and lead to treatments that target shared molecular pathways, offering broad benefits for preventing or slowing both metabolic disorders and cancer.
Abstract
Microinflammation serves as a central mechanism linking metabolic diseases and cancer. This study integrates gene expression profiles from irritable bowel syndrome (IBS), obesity, type 2 diabetes (T2D), colorectal cancer (CRC), renal cell carcinoma (RCC), and pancreatic cancer (PC) to identify shared molecular drivers of inflammation-mediated pathology. Weighted gene co-expression network analysis (WGCNA) revealed three highly preserved modules (blue, brown, turquoise) enriched in RNA processing, spliceosome assembly, ribosome biogenesis, and proteostasis regulation. Key hub genes, along with regulatory miRNAs have interconnected networks that modulate transcription, mRNA maturation, protein synthesis, and inflammatory signaling. Although classical inflammatory pathways were not directly enriched, their activity appears to be indirectly shaped by disruptions in RNA-processing and proteostasis machinery. Additionally, gut microbiota-derived products and altered metabolic states may further reinforce these transcriptional and post-transcriptional imbalances. Collectively, these findings reveal conserved molecular signatures that bridge microinflammation, metabolic disease, and oncogenesis, and highlight potential diagnostic and therapeutic targets centered on RNA regulation, proteostasis, and miRNA-mediated control