The pathogenesis of colorectal cancer is closely linked to immune regulation within the tumor microenvironment (TME). In this complex setting, neutrophils, as key components of the innate immune system, exhibit remarkable heterogeneity and functional plasticity. Recent studies have demonstrated that tumor-associated neutrophils (TANs) play a dual role in inflammation-driven tumorigenesis, angiogenesis, immune suppression, and the formation of a metastatic microenvironment in colorectal cancer, primarily through the release of cytokines, proteases, and reactive oxygen species (ROS), as well as the formation of neutrophil extracellular traps (NETs). Their specific functions are not a simple "either-or" dichotomy but rather represent a functional continuum dynamically shaped by intricate signaling networks within the TME. This article provides a systematic review of the molecular regulatory networks, clinical relevance, and therapeutic potential of TANs in the initiation and progression of colorectal cancer. Furthermore, we conclude that future research should focus on elucidating the characteristics of different TAN subsets, the mechanisms underlying their functional polarization, and how targeted interventions can improve the prognosis of colorectal cancer patients, thereby offering novel strategies and references for the clinical prevention and treatment of this disease.