{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE341nnn/GSE341968/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Homo sapiens"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE341968"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"TSPAN8 a plasticity marker is transcriptionally regulated through DUSP19 BRD4 crosstalk in Prostate Cancer cells","description":"To identify upstream regulators of TSPAN8 transcription, we screened a library of 298 phosphatases using a GFP reporter under the control of the TSPAN8 promoter in PC3 cells. DUSP19 emerged as the strongest negative regulator. Unexpectedly, DUSP19-mediated regulation of TSPAN8 was independent of its canonical JNK pathway: pharmacological JNK inhibition with SP600125 did not affect TSPAN8 expression, and pJNK/JNK levels were unchanged by siDUSP19. RNA-seq combined with promoter binding-site analysis identified BRD4 as the candidate effector linking DUSP19 to TSPAN8 transcription, and pharmacological BRD4 inhibition (AZD5153) reversed the siDUSP19-induced TSPAN8 upregulation at both mRNA and protein levels. Additionally, TSPAN8 accumulation is significantly higher in biopsies SYNAPTOPHYSIN+.","dates":{"publication":"2026/08/04"},"accession":"GSE341968","cross_references":{"GSM":["GSM9921018","GSM9921017","GSM9921016","GSM9921015","GSM9921020","GSM9921019"],"GPL":["23227"],"GSE":["341968"],"taxon":["Homo sapiens"]}}