The relationship between Porphyromonas gingivalis and oesophageal squamous cell carcinoma: a literature review.

Oesophageal cancer is the most common gastrointestinal malignancy in China and one of the major causes of death due to cancer worldwide. The occurrence of oesophageal cancer is a multifactor, multistage, and multistep process influenced by heredity, the environment, and microorganisms. Specifically, bacterial infection may be involved in the process of tissue carcinogenesis by directly or indirectly influencing tumour occurrence and development. Porphyromonas gingivalis is an important pathogen causing periodontitis, and periodontitis can promote the occurrence of various tumours. An increasing number of studies to date have shown that P. gingivalis plays an important role in the occurrence and development of oesophageal cancer. Overall, exploring how P. gingivalis promotes oesophageal cancer occurrence and development and how it affects the prognosis of these patients is of great importance for the diagnosis, prevention, and treatment of this type of cancer. Herein, the latest progress is reviewed.

Porphyromonas gingivalis promotes malignancy and chemo-resistance via GSK3ß-mediated mitochondrial oxidative phosphorylation in human esophageal squamous cell carcinoma.

Our prior studies have confirmed that long-term colonization of Porphyromonas gingivalis (Pg) and overexpression of the inflammatory factor glycogen synthase kinase 3ß (GSK3ß) promote the malignant evolution of esophageal squamous cell carcinoma (ESCC). We aimed to investigate the functional mechanism by which Pg could promote ESCC malignancy and chemo-resistance through GSK3ß-mediated mitochondrial oxidative phosphorylation (mtOXPHOS), and the clinical implications. The effects of Pg and GSK3ß on mtOXPHOS, malignant behaviors and response to paclitaxel and cisplatin treatment of ESCC cells were evaluated by in vitro and in vivo studies. The results showed that Pg induced high expression of the GSK3ß protein in ESCC cells and promoted the progression and chemo-resistance via GSK3ß-mediated mtOXPHOS in human ESCC. Then, Pg infection and the expression of GSK3ß, SIRT1 and MRPS5 in ESCC tissues were detected, and the correlations between each index and postoperative survival of ESCC patients were analysed. The results showed that Pg-positive ESCC patients with high-expression of GSK3ß, SIRT1 and MRPS5 have significant short postoperative survival. In conclusion, we demonstrated that the effective removal of Pg and inhibition of its promotion of GSK3ß-mediated mtOXPHOS may provide a new strategy for ESCC treatment and new insights into the aetiology of ESCC.