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TSPAN8 a plasticity marker is transcriptionally regulated through DUSP19 BRD4 crosstalk in Prostate Cancer cells

GSE341968 Homo sapiens Expression profiling by high throughput sequencing 6 samples Submitted 2026/08/04 Platform GPL23227
Summary
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+.
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Also filed as BioProject PRJNA1504923 and SRA study SRP722832. Searching any of these in the dataset finder brings you back here.

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