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Regulation of MEK inhibitor selumetinib sensitivity by AKT phosphorylation in the novel BRAF L525R mutant.

Chikako NakaiSachiyo MimakiKoutatsu MatsushimaEiji ShinozakiKentaro YamazakiKei MuroKensei YamaguchiTomohiro NishinaSatoshi YukiKohei ShitaraHideaki BandoYutaka SuzukiKiwamu AkagiShogo NomuraSatoshi FujiiMasaya SugiyamaNao NishidaMasashi MizokamiYasuhiro KohTakuya KoshizakaHideki OkadaYukiko AbeAtsushi OhtsuTakayuki YoshinoKatsuya Tsuchihara
Published in: International journal of clinical oncology (2023)
We established a model system harboring BRAF L525R using HEK293 cells. BRAF L525R constitutively activated ERK. AKT phosphorylation caused sensitivity and resistance to selumetinib. Our results suggest that a comprehensive network analysis may provide insights to identify effective therapies.
Keyphrases
  • signaling pathway
  • network analysis
  • wild type
  • induced apoptosis
  • cell proliferation
  • pi k akt
  • metastatic colorectal cancer
  • cell cycle arrest
  • protein kinase