| The pathogenesis of colorectal cancer has entered a new era of multidimensional host-environment-microecology interactions. Gut dysbiosis and the pathological remodeling of co-metabolic networks play a pivotal role in driving colorectal carcinogenesis, distant metastasis, and immune evasion. This review systematically elucidates the pro-tumor mechanisms of key pathogenic bacteria, such as Fusobacterium nucleatum and pks pathogenicity island-carrying Escherichia coli, which induce genomic instability and remodel the immunosuppressive microenvironment; contrastingly, it dissects the systemic defense networks constructed by core probiotics via metabolites such as short-chain fatty acids. Special emphasis is placed on the double-edged sword effects of microecological metabolic reprogramming, particularly the molecular pathways through which secondary bile acids drive metastasis via the gut-liver axis and ultra-long-chain C26 ceramides promote tumor proliferation. From the perspective of clinical translation, this review prospectively summarizes early non-invasive diagnostic models based on multimodal machine learning, alongside emerging microecological interventions encompassing fecal microbiota transplantation, precision phage therapy, and drug repurposing targeting specific metabolic enzymes. As microecological interventions transition from traditional broad-spectrum modulation to a precision-targeted paradigm, this review aims to provide robust theoretical support for overcoming clinical immunotherapy resistance and advancing individualized microbiota-targeted therapeutics in colorectal cancer. |
