TABLE 1.

Mechanisms associated with CRC progression induced by intestinal microbes.

Organism	The role for CRC	Mechanism	References
Fusobacterium nucleatum	Promote	• Regulates the E-cadherin/β-catenin signaling pathway and promotes tumor cell proliferation. • Activation of NF-κB pathway/RAS-MAPK pathway via MYD88 enhances CRC cell proliferation. • Increased H3K27ac histone modification in CRC cells, which activates glycolysis and carcinogenesis in CRC. • Activation of the NF-κB pathway/Recruits bone marrow-derived immune cells for CRC development. • Inhibits NK cell and T cell activity/Promotes M2-like polarization of macrophages to promote tumor immune escape. • Increased levels of Fusobacterium nucleatum promoted microsatellite instability (MSI) with CpG island methylation phenotype (CIMP) in CRC. • Activation of the TLR4/AKT/Keap1/NRF2 signaling pathway increases the production of 12 and 13-EpOME and promotes CRC metastasis. • Activation of autophagy to induce chemoresistance.	Kostic et al., 2013; Tahara et al., 2014; Gur et al., 2015; Sivan et al., 2015; Wang and Huycke, 2015; Abed et al., 2016; Mima et al., 2017; Yu et al., 2017; Chen et al., 2018, 2020; Rubinstein et al., 2019; Hong et al., 2021; Hu et al., 2021; Zheng et al., 2021
Escherichia coli	Promote	• DNA damage • Increased IL-17c expression and inhibited tumor cell apoptosis by increasing bcl-2 and bcl-xl expression. • Pro-inflammatory infiltrate	Cuevas-Ramos et al., 2010; Song et al., 2014; Yu and Fang, 2015; Veziant et al., 2016; Bertocchi et al., 2021; Dalal et al., 2021; Lee et al., 2021
ETBF	Promote	• Release of BFT, leading to E-cadherin cleavage with intestinal epithelial cell detachment and disruption of the intestinal epithelial barrier. • Th17 immune response, promotes IL-6, TNF-α production, activates STAT3, NF-kB signaling pathway and promotes tumorigenesis. • DNA damage.	Destefano Shields et al., 2011; Goodwin et al., 2011; DeDecker et al., 2021
Escherichia coli	Promote	• It leads to CIN in epithelial progenitor cells, resulting in gene mutations.	Wang et al., 2015; Wang and Huycke, 2015