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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.
2025-08-20 | GSE300839 | GEO
Project description:Azonexaceae bacterium 9S strain:9S Genome sequencing
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Project description:To compare secretory signatures of wildtype and mutant mice, the transcription profiles of tdTom+ cells from Atoh1(WT)CreERT2 R26RtdTom and Atoh1(9S/T-A)CreERT2 R26RtdTom mice were generated. The profiles were obtained for both small intestine (SI) and colon.
2018-08-06 | GSE115367 | GEO
Project description:Both genetic and environmental factors are implicated in Type 1 Diabetes (T1D). Since environmental factors can trigger epigenetic changes, we hypothesized that variations in histone posttranslational modifications (PTMs) at the promoter/enhancer regions of T1D susceptible genes may be associated with T1D. We therefore evaluated histone PTM variations at known T1D susceptible genes in blood cells from T1D patients versus healthy non-diabetic controls, and explored their connections to T1D. We used the chromatin-immunoprecipitation-linked-to-microarray approach to profile key histone PTMs, including H3-lysine-4 trimethylation (H3K4me3), H3K27me3, H3K9me3, H3K9 acetylation (H3K9Ac) and H4K16Ac at genes within the T1D susceptible loci in lymphocytes, and H3K4me3, H3K9me2, H3K9Ac and H4K16Ac at the IDDM1 region in monocytes of T1D patients and healthy controls separately. We screened for potential variations in histone PTMs using computational methods to compare datasets from T1D and controls. Interestingly, we observed marked variations in H3K9Ac levels at the upstream regions of HLA-DRB1 and HLA-DQB1 within the IDDM1 locus in T1D monocytes relative to controls. Additional experiments with THP-1 monocytes demonstrated increased expression of HLA-DRB1 and HLA-DQB1 in response to interferon- and TNF-treatment that were accompanied by changes in H3K9Ac at the same promoter regions as that seen in the patient monocytes. These results suggest that the H3K9Ac status of HLA-DRB1 and HLA-DQB1, two genes highly associated with T1D, may be relevant to their regulation and transcriptional response towards external stimuli. Thus, the promoter/enhancer architecture and chromatin status of key susceptible loci could be important determinants in their functional association to T1D susceptibility.
2012-06-01 | GSE36397 | GEO