miR-135a-5p-mediated downregulation of protein tyrosine phosphatase receptor delta is a candidate driver of HCV-associated hepatocarcinogenesis.
Nicolaas Van RenneArmando Andres Roca SuarezFrancois H T DuongClaire GondeauDiego CalabreseNelly FontaineAmina AbabsaSimonetta BandieraTom CroonenborghsNathalie PochetVito De BlasiPatrick PessauxTullio PiardiDaniele SommacaleAtsushi OnoKazuaki ChayamaMasashi FujitaHidewaki NakagawaYujin HoshidaMirjam B ZeiselMarkus H HeimThomas F BaumertJoachim LupbergerPublished in: Gut (2017)
We previously demonstrated that STAT3 is required for HCV infection. We conclude that HCV promotes a STAT3 transcriptional programme in the liver of patients by suppressing its regulator PTPRD via upregulation of miR-135a-5p. Our results show the existence of a perturbed PTPRD-STAT3 axis potentially driving malignant progression of HCV-associated liver disease.
Keyphrases
- hepatitis c virus
- cell proliferation
- human immunodeficiency virus
- end stage renal disease
- ejection fraction
- transcription factor
- chronic kidney disease
- signaling pathway
- gene expression
- prognostic factors
- randomized controlled trial
- binding protein
- clinical trial
- patient reported outcomes
- heat shock protein
- protein kinase
- antiretroviral therapy