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Commensal Lactobacillus Suppress Colon Tumorigenesis and Progression by Modulation of Sphingosine 1-Phosphate Signaling in Mice

Fuqiang Xu,Qiaoqiao Li,Shu-Yang Wang,Miaoyin Dong,G. Xiao,Jin Bai,Junkai Wang,Xisi Sun

Published 2022 in Unknown venue

ABSTRACT

Background: Gut microbiota and their secreted metabolites influence the initiation, progression, and treatment responsiveness of colon cancer. Microbiota-based therapy regulated by probiotics has been considered as an effective strategy for prevention and therapeutic of colon cancer, whereas the antitumor mechanisms influenced by microbiota and their metabolites with intervention of probiotic remain further investigated.Results: Here, we investigated the preventive and therapeutic efficiency of commensal Lactobacillus in subcutaneous tumor models, and the underlying antitumor mechanism through the alteration of gut microbiota and their metabolites regulated by commensal Lactobacillus. Interestingly, we found that tumor formation rate in subcutaneous tumor models reduced 86.21% and 82.76%, in comparison to tumor controls when administrated with living or inactivated Lactobacillus (JY300-8 and JMR-01) for 20 days in advance. Subsequently, continuously oral administration for living or inactivated commensal Lactobacillus suppressed significantly the growth of tumor, and the tumor volumes declined 65.2% and 61.18%, respectively. Furthermore, microbiome and metabolome analyses revealed that commensal Lactobacillus suppressed colon tumorigenesis and progression through the modulation of gut microbiota and metabolites which included the down-regulation of secondary bile acids, sphingosine 1-phosphate (S1P) signaling in cancer and pyrimidine metabolism, as well as the production of anticarcinogenic compounds in tumor-bearing mice. Particularly, limitation the effects of S1P signaling via the modulation of sphingosine expression using probiotics, exerted antitumor efficiency.Conclusions: The work indicated the feasibility of using an effectively safe strategy to prevent the occurrence of colon cancer, and provided a potential therapeutic target for new therapeutics strategy via altering S1P signaling in cancer.

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