ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/021/SRR28560221/SRR28560221_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/024/SRR28560224/SRR28560224_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/025/SRR28560225/SRR28560225_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/020/SRR28560220/SRR28560220_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/023/SRR28560223/SRR28560223_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/020/SRR28560220/SRR28560220_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/026/SRR28560226/SRR28560226_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/019/SRR28560219/SRR28560219_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/025/SRR28560225/SRR28560225_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/022/SRR28560222/SRR28560222_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/029/SRR28560229/SRR28560229_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/028/SRR28560228/SRR28560228_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/031/SRR28560231/SRR28560231_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/019/SRR28560219/SRR28560219_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/023/SRR28560223/SRR28560223_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/031/SRR28560231/SRR28560231_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/030/SRR28560230/SRR28560230_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/029/SRR28560229/SRR28560229_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/027/SRR28560227/SRR28560227_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/026/SRR28560226/SRR28560226_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/022/SRR28560222/SRR28560222_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/024/SRR28560224/SRR28560224_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/030/SRR28560230/SRR28560230_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/028/SRR28560228/SRR28560228_2.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/027/SRR28560227/SRR28560227_1.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR285/021/SRR28560221/SRR28560221_1.fastq.gzprimaryOK200GenomicsMakowski Lab CRB 322, Medicine- Heme Onc, UTHSChttps://www.ebi.ac.uk/ena/browser/view/PRJNA1096356Mus musculusBreast cancer (BC) is the most common malignancy and the leading cause of cancer mortality in women. It is possible that signals arising from the gut microbiome are protective in BC. We used common drugs designed to turn on pathways to mimic one major signal coming from gut microbes, namely bile acids. Taking advantage of a drug called Ocaliva, which is commercially available for another disease, we repurposed this drug to test its anti-cancer potential. Ocaliva worked on a specific protein target called FXR to reduce tumor growth and kill cancer cells. In contrast, a similar drug that targets a different protein called TGR5 was not effective in killing cancer cells. Taken together, these findings suggest that using Ocaliva or other bile acid signals derived from the gut microbiome to target the protein FXR could be an important new therapeutic strategy for individuals with aggressive BC. Overall design: RNA -Seq data from bulk tumor (orthotopically injected with MDAMB231 Human Triple Negative Breast Cancer Cells) in NSG immunocompetent mice, treated with vehicle (40% DMSO and& 60% polyethylene glycol (PEG), N = 8), OCA (30 mg/kg "mpk", N = 7), or chemotherapy paclitaxel (“Ptax”, 10 mg/kg "mpk", N = 6), grown for 14 days, excised and Snap frozen.ENAfalseFXR Agonism with Bile Acid Mimetic Reduces Pre-Clinical Triple-Negative Breast Cancer BurdenFXR Agonism with Bile Acid Mimetic Reduces Pre-Clinical Triple-Negative Breast Cancer Burden2025-09-242024-04-07PRJNA1096356GSE26325510090