Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1036002 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Obesity is predicted to become the largest modifiable risk factor for breast cancer in postmenopausal women, yet the mechanisms underlying this association are unclear. We identified a novel protective mechanism for lean adipocytes to suppress breast cancer by secreting the oxylipin 9S-HODE, which induces ferroptosis in breast cancer cells while sparing normal breast epithelial cells. Consequently, the inhibition of ferroptosis accelerates breast cancer in lean, but not obese, mice. Obese adipocytes fail to secrete 9S-HODE, suggesting that the loss of 9S-HODE significantly contributes to the acceleration of breast cancer in obesity. Further, 9S-HODE supplementation into tumors in obese mice is sufficient to reduce tumor burden and additionally can inhibit the growth of patient-derived breast cancer organoids, underscoring its potential as a therapeutic agent.
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Project description:Azonexaceae bacterium 9S strain:9S Genome sequencing
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Project description:Interventions: different phenotypes vs. HNPCC group vs. healthy control group:Nil
Primary outcome(s): Alpha diversity analysis;ß-diversity analysis;LDA EffectSize (LEfSe) analysis
Study Design: Factorial
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Project description:Opioids such as morphine have many beneficial properties as analgesics, however, opioids may induce multiple adverse gastrointestinal symptoms. We have recently demonstrated that morphine treatment results in significant disruption in gut barrier function leading to increased translocation of gut commensal bacteria. However, it is unclear how opioids modulate the gut homeostasis. By using a mouse model of morphine treatment, we studied effects of morphine treatment on gut microbiome. We characterized phylogenetic profiles of gut microbes, and found a significant shift in the gut microbiome and increase of pathogenic bacteria following morphine treatment when compared to placebo. In the present study, wild type mice (C57BL/6J) were implanted with placebo, morphine pellets subcutaneously. Fecal matter were taken for bacterial 16s rDNA sequencing analysis at day 3 post treatment. A scatter plot based on an unweighted UniFrac distance matrics obtained from the sequences at OTU level with 97% similarity showed a distinct clustering of the community composition between the morphine and placebo treated groups. By using the chao1 index to evaluate alpha diversity (that is diversity within a group) and using unweighted UniFrac distance to evaluate beta diversity (that is diversity between groups, comparing microbial community based on compositional structures), we found that morphine treatment results in a significant decrease in alpha diversity and shift in fecal microbiome at day 3 post treatment compared to placebo treatment. Taxonomical analysis showed that morphine treatment results in a significant increase of potential pathogenic bacteria. Our study shed light on effects of morphine on the gut microbiome, and its role in the gut homeostasis.
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