Construction of Model Animals to Explore Intestinal Microbiome for Detection of Breast Cancer

Abstract

Breast cancer ranks first among female cancers and has become a major public health problem in the current society. More studies indicated that these cancers are related to the change in the gut microbiome that can cause metabolic and immune system disorders in the body. However, there are few studies on the changes in gut microbiome caused by the onset of breast cancer, and the relationship between breast cancer and gut microbiome needs to be further clarified. In this study, we inoculated 4T1 breast cancer cells to induce breast cancer tumorigenesis in mice and collected their feces samples at different stages during this process. These intestinal florae were analyzed using 16S rRNA gene amplicon sequencing, and the results showed that at the phylum level, the ratio of Firmicutes/Bacteroidetes decreased with the development of the tumor; at the family level, the intestinal microbiome had obvious variations of Lachnospiraceae, Bacteroidaceae, Erysipelotrichaceae, etc. The Kyoto Encyclopedia of Genes and Genomes (KEGG) and COG annotation demonstrated that decreased abundance of cancer related signaling pathways. This study elucidated the relationship between breast cancer and intestinal microbiome, and the research results can be used as an important biomarker for the diagnosis of breast cancer.

Metabolome–microbiome insights into therapeutic impact of 8‐O‐acetylharpagide against breast cancer in a murine model

“…These correlation results are consistent with our results on gut microbiota and prostaglandin G2 metabolism after 8‐ O‐ acetylharpagide treatment. Moreover, it has been shown that Lachnospiraceae is negatively correlated with AA (Luo et al, 2020) and that AA produces prostaglandin G2 via the cyclooxygenase pathway, and the relative abundance of Lachnospiraceae was significantly increased in BC model mice (Ji et al, 2023). These data suggest that the gut microbiota may play an important role in the regulation of AA and prostaglandin G2.…”