Intracellular Promotes the Proliferation of Colorectal Cancer Cells the MAPK/ERK Signaling Pathway.

() is a keystone pathogen in periodontitis. However, several clinical studies have revealed an enrichment of in the stool samples and colorectal mucosa of colorectal cancer patients. Thus, the goal of this study was to determine whether can promote colorectal cancer progression . We established an acute infection model (24 h, multiplicity of infection =100) of invasion of colorectal cancer cells to study the alterations induced by in the proliferation and cell cycle of colorectal cancer cells. We observed that can adhere and invade host cells a few hours after infection. Once invaded, significantly promoted colorectal cancer cell proliferation, and the percentage of S phase cells was increased in the cell cycle assay. However, KDP136, a gingipain-deficient mutant of 33277, showed a decreased ability to promote colorectal cancer cell proliferation, indicating that gingipain is associated with colorectal cancer cell proliferation. Furthermore, we extracted RNA from colorectal cancer cells for high-throughput sequencing analysis and reconfirmed the results by quantitative polymerase chain reaction and western blot analyses. The results suggested that the MAPK/ERK signaling pathway is significantly activated by , while these changes were not observed for KDP136. In conclusion, can invade cells and promote the proliferation of colorectal cancer cells by activating the MAPK/ERK signaling pathway. Gingipain is an essential virulence factor in this interaction.