The collective group of bacteria, fungi, viruses, Protista, and Archaea predominantly regulate the gastrointestinal tract and produce metabolites for a lifetime. The gut microbiota affects several processes, such as colonization, pathogen resistance, intestinal epithelium maintenance, metabolism of food and medication, immune function regulation, and behavior regulation. Humans contain trillions of different microbiotas, but in the case of dysbiosis, a change in microbiota from healthy to unhealthy promotes disease condition. Dysbiosis can be altered by certain factors such as antibiotics, drugs, diet, genetics, physical and psychological stress, etc. Dysbiosis is the main responsible key to colorectal cancer. The gut microbiota influences epigenetic modifications in colorectal carcinogenesis. The Pathogenic bacteria can replace harmless commensal bacteria such as Lactobacillus, Bacteroides, E. coli, and S. epidermidis, causing inflammation in the host, promoting cell proliferation, and inducing carcinogenic signals and metabolites. Strategies of gut microbiota modulation are explained in this topic, such as postbiotics, probiotics, prebiotics, nutraceuticals, mucosal immunomodulation, enhancement of gut barrier function, gene therapy, dietary habits, microbiota and CRC RT, fecal microbiota transplantation, and drugs. Interaction between intestinal flora and colorectal cancer with a detailed explanation of this can stimulate inflammation and promote tumor formation through many inflammation-related signaling pathways such as NF-κB, STAT3, Wnt/β-catenin epigenetic changes, and carcinogenetic changes. It is found to be the impact of gut microbiota on treatment toxicity in CRC with inhibition of CRC proliferation but also induces its metastasis via succinate receptor signaling.