Fusobacterium nucleatum-induced imbalance in microbiome-derived butyric acid levels promotes the occurrence and development of colorectal cancer

Figure 8 Sodium butyrate and Fusobacteriumnucleatum regulates the proliferation of colorectal cancer cells through the adenosine monophosphate-activated protein kinase signal pathway. A and B: Adenosine monophosphate-activated protein kinase (AMPK) was activated in DLD-1 and HCT116 cells by treatment with sodium butyrate (NaB), leading to increased expression of phosphorylated AMPK (p-AMPK), decrease in expression of proliferation proteins such as CDK1, C-myc, and cyclin B1, and increase in expression of cycle arrest protein P21. However, treatment with Fusobacterium nucleatum inhibited the expression of p-AMPK. Data are expressed as mean ± standard deviation, from at least three independent experiments. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001, ns: P > 0.05.