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LncRNA AK023948 is a positive regulator of AKT

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Listed:
  • Pratirodh Koirala

    (Cancer Institute, University of Mississippi Medical Center
    University of Mississippi Medical Center)

  • Jianguo Huang

    (Cancer Institute, University of Mississippi Medical Center
    University of Mississippi Medical Center)

  • Tsui-Ting Ho

    (Cancer Institute, University of Mississippi Medical Center
    University of Mississippi Medical Center
    University of Mississippi Medical Center)

  • Fangting Wu

    (System Biosciences)

  • Xianfeng Ding

    (Cancer Institute, University of Mississippi Medical Center
    College of Life Sciences, Zhejiang Sci-Tech University)

  • Yin-Yuan Mo

    (Cancer Institute, University of Mississippi Medical Center
    University of Mississippi Medical Center)

Abstract

Despite the overwhelming number of human long non-coding RNAs (lncRNAs) reported so far, little is known about their physiological functions for the majority of them. The present study uses a CRISPR/Cas9-based synergistic activation mediator (SAM) system to identify potential lncRNAs capable of regulating AKT activity. Among lncRNAs identified from this screen, we demonstrate that AK023948 is a positive regulator for AKT. Knockout of AK023948 suppresses, whereas rescue with AK023948 restores the AKT activity. Mechanistically, AK023948 functionally interacts with DHX9 and p85. Importantly, AK023948 is required for the interaction between DHX9 and p85 to hence the p85 stability and promote AKT activity. Finally, AK023948 is upregulated in breast cancer; interrogation of TCGA data set indicates that upregulation of DHX9 in breast cancer is associated with poor survival. Together, this study demonstrates two previously uncharacterized factors AK023948 and DHX9 as important players in the AKT pathway, and that their upregulation may contribute to breast tumour progression.

Suggested Citation

  • Pratirodh Koirala & Jianguo Huang & Tsui-Ting Ho & Fangting Wu & Xianfeng Ding & Yin-Yuan Mo, 2017. "LncRNA AK023948 is a positive regulator of AKT," Nature Communications, Nature, vol. 8(1), pages 1-10, April.
    • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms14422
    DOI: 10.1038/ncomms14422
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