Porphyromonas gingivalis (P. gingivalis) is a keystone pathogen in periodontitis. However, several clinical studies have revealed an enrichment of P. gingivalis in the stool samples and colorectal mucosa of colorectal cancer patients. Thus, the goal of this study was to determine whether P. gingivalis can promote colorectal cancer progression in vitro. We established an acute infection model (24 h, multiplicity of infection =100) of P. gingivalis invasion of colorectal cancer cells to study the alterations induced by P. gingivalis in the proliferation and cell cycle of colorectal cancer cells. We observed that P. gingivalis can adhere and invade host cells a few hours after infection. Once invaded, P. gingivalis 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 P. gingivalis 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 P. gingivalis, while these changes were not observed for KDP136. In conclusion, P. gingivalis 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.

牙龈卟啉单胞菌 （牙龈卟啉单胞菌）是牙周炎的关键病原体。但是，一些临床研究表明，牙龈卟啉单胞菌在大肠癌患者的粪便样本和大肠黏膜中。因此，这项研究的目的是确定牙龈卟啉单胞菌 可以促进大肠癌的进展 体外。我们建立了一个急性感染模型（24小时，感染复数= 100）牙龈卟啉单胞菌 侵袭大肠癌细胞以研究其诱导的改变 牙龈卟啉单胞菌在大肠癌细胞的增殖和细胞周期中的作用。我们观察到牙龈卟啉单胞菌可以在感染后几个小时粘附并侵袭宿主细胞。一旦入侵，牙龈卟啉单胞菌显着促进了结肠直肠癌细胞的增殖，并且在细胞周期测定中增加了S期细胞的百分比。但是，KDP136是一种缺乏姜黄素的突变体牙龈卟啉单胞菌33277显示出促进结肠直肠癌细胞增殖的能力降低，表明姜黄素与结肠直肠癌细胞增殖有关。此外，我们从结肠直肠癌细胞中提取RNA进行高通量测序分析，并通过定量聚合酶链反应和Western blot分析再次确认了结果。结果表明，MAPK / ERK信号通路被下列物质显着激活：牙龈卟啉单胞菌，而KDP136未观察到这些变化。结论，牙龈卟啉单胞菌可以通过激活MAPK / ERK信号通路侵入细胞并促进结直肠癌细胞的增殖。姜黄素是这种相互作用中必不可少的毒力因子。