Oncogenic combined calcineurin-nuclear factor of activated T cells and toll-like receptor signals in colon

Inflammation is emerging as one of the hallmarks of cancer pathogenesis and progression; its role in many tumors still remains unclear. Increasing evidences suggest that acute and chronic intestinal inflammation and activation of inflammation-associated pathways contribute to the pathogenesis of colorectal cancer (CRC) (1,2). Long-term treatment with non-steroidal anti-inflammatory drugs is able to remarkably reduce the CRC rate and death, and CRC development and progression are often associated with dysbiosis, a broad change of intestinal microbiota stratification and enrichment of certain microbial strains. However, the molecular mechanisms how inflammatory-related cascades promote CRC development are still uncovered.