Zhengdong Yang, Xinyang Wang, Huiying Zhou, Minghan Jiang, Jinghui Wang, Bowen Sui

The First Department of Oncology, Heilongjiang University of Chinese Medicine, Heilongjiang, 150040, People’s Republic of China

Correspondence: Bowen Sui, The First Department of Oncology, Heilongjiang University of Chinese Medicine, Heilongjiang, 150001, People’s Republic of China, Email suibowen79@sina.com

Abstract: Colorectal cancer (CRC) is a diverse disease entity and a leading cause of cancer-related mortality worldwide. CRC results from the accumulation of multiple genetic and epigenetic alterations. This heterogeneity of CRC underscores the significance of understanding its molecular landscape, as variations in tumor genetics can greatly influence both patient prognosis and therapeutic response. The molecular complexity of CRC is defined by three major carcinogenesis pathways: chromosomal instability (CIN), microsatellite instability (MSI), and the CpG island methylator phenotype (CIMP). These pathways contribute to the onset and progression of CRC through mutations, epigenetic modifications, and dysregulated cellular signalling networks. The heterogeneous nature of CRC continues to pose challenges in identifying universally effective treatments, highlighting the need for personalized approaches. Hence, the present review aims at unravelling the molecular complexity of CRC that is essential for improving diagnosis, prognostication, and treatment. We detail on the current understanding of the molecular framework of CRC, central signalling pathways of CRC associated with its initiation to a malignant phenotype, further invasion, progression, metastases, and response to therapy. Continued research into CRC’s pathways and biomarkers will pave the way for the development of more precise and effective therapeutic strategies, ultimately improving patient outcomes.

Keywords: colorectal cancer, molecular mechanisms, pathways, chromosomal instability, adenomatous polyposis coli, biomarkers