Enterocloster bolteae drives hyperglycemia-associated colorectal cancer cell proliferation via Rac/Rho-MSH6-Elongin C signaling pathway

Figure 7 Effects of Enterocloster bolteae treatment on gene expression in LoVo and RKO colorectal cancer cells. A P value < 0.05 indicates statistically significant differences. All data were normalized to the glyceraldehyde-3-phosphate dehydrogenase endogenous control. Error bars represent standard error of the mean from triplicate experiments. Statistical analysis was performed using one-way analysis of variance with Dunnett’s post-test. Colon cancer cells were treated with Enterocloster bolteae supernatant at a 1:10 ratio (bacterial supernatant to high-glucose Dulbecco’s modified Eagle’s medium) for 24 hours. Compared with controls, relative mRNA expression levels of different targets in LoVo and RKO colorectal carcinoma cell lines were assessed by quantitative real-time polymerase chain reaction. A: 16S rDNA sequence from the Ribosomal Database Project (http://rdp.cme.msu.edu/index.jsp). The comparison results indicate that the strain is Enterocloster bolteae (formerly Clostridium bolteae); B: DNA target band obtained by excising the electrophoresis band of polymerase chain reaction products; C and D: Relative mRNA expression levels of Rho, Rac, hMSH6, Elongin C (ELOC/TCEB1), and TRK in LoVo (Figure 7C) and RKO (Figure 7D) colorectal carcinoma cell lines, as assessed by quantitative real-time polymerase chain reaction.