Abstract

Abstract Periodontal disease has been shown to play important roles in the pathogenesis of many chronic diseases. Recent epidemiological studies and microbiome analysis have suggested that periodontal disease may be associated with the progression of pancreatic cancer. Our recent study has demonstrated that oral-smear of a periodontitis pathogen Porphyromonas gingivalis (P. gingivalis) significantly induced pancreatic cancer deterioration in the KrasG12D/-Pdx-1-Cre transgenic mouse model. Higher expression levels of epithelial-mesenchymal transition (EMT) markers, such as N-Cadherin, αSMA, SNAIL-1, Vimentin and ZEB1, were observed in P. gingivalis-treated KrasG12D/-Pdx-1-Cre mice than the untreated controls. In an attempt to develop a prophylactic treatment for pancreatic cancer, the mice were fed with a combination of two probiotics, Lactobacillus reuteri and Lactobacillus paracasei, for four consecutive weeks after oral-smear of P. gingivalis. These probiotic strains have been demonstrated to have the efficacy of either anti-inflammation or enhancement of cell-mediated immunity, respectively. Our results demonstrated that oral administration of the probiotics significantly suppressed oncogenic Kras-induced pancreatic cancer development and reversed P. gingivalis-stimulated cancer deterioration in mice. Significantly reduced expression of the aforementioned EMT markers in pancreatic cancer tissues was observed in KrasG12D/-Pdx-1-Cre transgenic mice treated with the probiotics. Our results suggest that the microbiota profile is very important for pancreatic cancer development. The manipulation of microbiota for enhancing antitumor immunity may be an emerging strategy for cancer prevention. Citation Format: Ming-Shiou Jan, Wan-Ting Chen, Yu-Jen Chen, Chia-Wei Lin, Wen-Wei Chang, Chung-Hung Tsai, Jia-Shiou Peng, Li-Jin Hsu. Probiotics ameliorate Porphyromonas gingivalis-promoted pancreatic cancer progression in oncogenic Kras transgenic mice [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 235. doi:10.1158/1538-7445.AM2017-235

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