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Interaction between MED12 and ΔNp63 activates basal identity in pancreatic ductal adenocarcinoma.
Maia-Silva, Diogo; Cunniff, Patrick J; Schier, Allison C; Skopelitis, Damianos; Trousdell, Marygrace C; Moresco, Philip; Gao, Yuan; Kechejian, Vahag; He, Xue-Yan; Sahin, Yunus; Wan, Ledong; Alpsoy, Aktan; Liverpool, Jynelle; Krainer, Adrian R; Egeblad, Mikala; Spector, David L; Fearon, Douglas T; Dos Santos, Camila O; Taatjes, Dylan J; Vakoc, Christopher R.
Afiliación
  • Maia-Silva D; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Cunniff PJ; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Schier AC; Department of Biochemistry, University of Colorado, Boulder, CO, USA.
  • Skopelitis D; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Trousdell MC; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Moresco P; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Gao Y; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Kechejian V; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • He XY; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Sahin Y; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Wan L; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Alpsoy A; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Liverpool J; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Krainer AR; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Egeblad M; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Spector DL; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Fearon DT; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Dos Santos CO; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
  • Taatjes DJ; Department of Biochemistry, University of Colorado, Boulder, CO, USA.
  • Vakoc CR; Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA. vakoc@cshl.edu.
Nat Genet ; 56(7): 1377-1385, 2024 Jul.
Article en En | MEDLINE | ID: mdl-38886586
ABSTRACT
The presence of basal lineage characteristics signifies hyperaggressive human adenocarcinomas of the breast, bladder and pancreas. However, the biochemical mechanisms that maintain this aberrant cell state are poorly understood. Here we performed marker-based genetic screens in search of factors needed to maintain basal identity in pancreatic ductal adenocarcinoma (PDAC). This approach revealed MED12 as a powerful regulator of the basal cell state in this disease. Using biochemical reconstitution and epigenomics, we show that MED12 carries out this function by bridging the transcription factor ΔNp63, a known master regulator of the basal lineage, with the Mediator complex to activate lineage-specific enhancer elements. Consistent with this finding, the growth of basal-like PDAC is hypersensitive to MED12 loss when compared to PDAC cells lacking basal characteristics. Taken together, our genetic screens have revealed a biochemical interaction that sustains basal identity in human cancer, which could serve as a target for tumor lineage-directed therapeutics.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Pancreáticas / Factores de Transcripción / Carcinoma Ductal Pancreático / Proteínas Supresoras de Tumor / Complejo Mediador Límite: Humans Idioma: En Revista: Nat Genet Asunto de la revista: GENETICA MEDICA Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neoplasias Pancreáticas / Factores de Transcripción / Carcinoma Ductal Pancreático / Proteínas Supresoras de Tumor / Complejo Mediador Límite: Humans Idioma: En Revista: Nat Genet Asunto de la revista: GENETICA MEDICA Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos