|Number of samples:||18|
|Release date:||Dec 7 2017|
|Last update date:||Nov 28 2018|
|Diseases:||Urinary Bladder Neoplasms, Neoplasms|
|Dataset link||Bladder-cancer-associated mutations in RXRA activate peroxisome proliferator-activated receptors to drive urothelial proliferation|
Two independent bladder cancer cell lines, JMSU-1 and 575A, were transfected with retrovirus to generate stable cell lines expressing either human wild-type RXRA (RXRAwt) or a mutant form of RXRA, RXRA S427F (RXRAS427F). RNA-seq was performed in biological triplicate on RXRAwt-expressing cells treated with vehicle or the PPARG agonist pioglitazone (pio), and RXRAS427F-expressing cells treated with vehicle. Fragments were sequenced on an Illumina HiSeq-2500 or HiSeq-3000. Transcriptomes in the wild-type and S427F conditions were compared to establish a causal role of the RXRA hot-spot mutation S427F in the hyper-activation of PPAR singling.
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