Loss of NDRG2 expression activates PI3K-AKT signalling via PTEN phosphorylation in ATLL and other cancers

نویسندگان

  • Shingo Nakahata
  • Tomonaga Ichikawa
  • Phudit Maneesaay
  • Yusuke Saito
  • Kentaro Nagai
  • Tomohiro Tamura
  • Nawin Manachai
  • Norio Yamakawa
  • Makoto Hamasaki
  • Issay Kitabayashi
  • Yasuhito Arai
  • Yae Kanai
  • Tomohiko Taki
  • Takaya Abe
  • Hiroshi Kiyonari
  • Kazuya Shimoda
  • Koichi Ohshima
  • Akira Horii
  • Hiroshi Shima
  • Masafumi Taniwaki
  • Ryoji Yamaguchi
  • Kazuhiro Morishita
چکیده

Constitutive phosphatidylinositol 3-kinase (PI3K)-AKT activation has a causal role in adult T-cell leukaemia-lymphoma (ATLL) and other cancers. ATLL cells do not harbour genetic alterations in PTEN and PI3KCA but express high levels of PTEN that is highly phosphorylated at its C-terminal tail. Here we report a mechanism for the N-myc downstream-regulated gene 2 (NDRG2)-dependent regulation of PTEN phosphatase activity via the dephosphorylation of PTEN at the Ser380, Thr382 and Thr383 cluster within the C-terminal tail. We show that NDRG2 is a PTEN-binding protein that recruits protein phosphatase 2A (PP2A) to PTEN. The expression of NDRG2 is frequently downregulated in ATLL, resulting in enhanced phosphorylation of PTEN at the Ser380/Thr382/Thr383 cluster and enhanced activation of the PI3K-AKT pathway. Given the high incidence of T-cell lymphoma and other cancers in NDRG2-deficient mice, PI3K-AKT activation via enhanced PTEN phosphorylation may be critical for the development of cancer.

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عنوان ژورنال:

دوره 5  شماره 

صفحات  -

تاریخ انتشار 2014