Serine/Threonine Kinase MLK4 Determines Mesenchymal Identity in Glioma Stem Cells in an NF-κB-dependent Manner.

نویسندگان

  • Sung-Hak Kim
  • Ravesanker Ezhilarasan
  • Emma Phillips
  • Daniel Gallego-Perez
  • Amanda Sparks
  • David Taylor
  • Katherine Ladner
  • Takuya Furuta
  • Hemragul Sabit
  • Rishi Chhipa
  • Ju Hwan Cho
  • Ahmed Mohyeldin
  • Samuel Beck
  • Kazuhiko Kurozumi
  • Toshihiko Kuroiwa
  • Ryoichi Iwata
  • Akio Asai
  • Jonghwan Kim
  • Erik P Sulman
  • Shi-Yuan Cheng
  • L James Lee
  • Mitsutoshi Nakada
  • Denis Guttridge
  • Biplab DasGupta
  • Violaine Goidts
  • Krishna P Bhat
  • Ichiro Nakano
چکیده

Activation of nuclear factor κB (NF-κB) induces mesenchymal (MES) transdifferentiation and radioresistance in glioma stem cells (GSCs), but molecular mechanisms for NF-κB activation in GSCs are currently unknown. Here, we report that mixed lineage kinase 4 (MLK4) is overexpressed in MES but not proneural (PN) GSCs. Silencing MLK4 suppresses self-renewal, motility, tumorigenesis, and radioresistance of MES GSCs via a loss of the MES signature. MLK4 binds and phosphorylates the NF-κB regulator IKKα, leading to activation of NF-κB signaling in GSCs. MLK4 expression is inversely correlated with patient prognosis in MES, but not PN high-grade gliomas. Collectively, our results uncover MLK4 as an upstream regulator of NF-κB signaling and a potential molecular target for the MES subtype of glioblastomas.

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عنوان ژورنال:
  • Cancer cell

دوره 29 2  شماره 

صفحات  -

تاریخ انتشار 2016