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ARID1A facilitates KRAS signaling-regulated enhancer activity in an AP1-dependent manner in colorectal cancer cells.

Madhobi SenXin WangFeda H HamdanJacobe RappJessica EggertRobyn Laura KosinskyFlorian WegwitzAna Patricia KutschatFereshteh S YounesiJochen GaedckeMarian GradeElisabeth HessmannArgyris PapantonisPhilipp StrӧbelSteven A Johnsen
Published in: Clinical epigenetics (2019)
We identify a previously unknown context-dependent tumor-supporting function of ARID1A in CRC downstream of KRAS signaling. Upon the loss of ARID1A in KRAS-mutated cells, enhancers that are co-occupied by ARID1A and the AP1 transcription factors become inactive, thereby leading to decreased target gene expression. Thus, targeting of the BAF complex in KRAS-mutated CRC may offer a unique, previously unknown, context-dependent therapeutic option in CRC.
Keyphrases
  • wild type
  • transcription factor
  • gene expression
  • induced apoptosis
  • dna methylation
  • dna binding
  • binding protein
  • cancer therapy
  • genome wide identification