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A cytoplasmic long noncoding RNA LINC00470 as a new AKT activator to mediate glioblastoma cell autophagy

Changhong Liu1,2,3,4, Yan Zhang1,2,3,4, Xiaoling She5

  • 1Hunan Provincial Tumor Hospital and the Affiliated Tumor Hospital of Xiangya Medical School, Central South University, Changsha, 410006, Hunan, China.

Journal of Hematology & Oncology
|June 6, 2018
PubMed
Abstract

Insights

This study reveals that LINC00470 activates AKT signaling in glioblastoma (GBM) by interacting with FUS. This pathway promotes GBM progression and indicates LINC00470

Area of Science:

  • Molecular Biology
  • Oncology
  • Biochemistry

Background:

  • The regulation of AKT signaling by long non-coding RNAs (lncRNAs) in glioblastoma (GBM) remains largely unexplored.
  • Understanding lncRNA involvement in AKT pathways is crucial for GBM research.

Purpose of the Study:

  • To investigate the role of LINC00470 in regulating AKT activation in GBM cells.
  • To elucidate the molecular mechanism by which LINC00470 influences GBM malignancy.

Main Methods:

  • RNA-binding protein immunoprecipitation (RIP) and RNA pulldown assays to confirm LINC00470-FUS binding.
  • Co-immunoprecipitation (Co-IP) and GST pulldown assays to detect FUS-AKT interactions.
  • EdU, CCK-8, and intracranial xenograft assays to assess LINC00470's effect on GBM.
  • RT-qPCR and Western blotting to analyze AKT and pAKT levels.

Main Results:

  • LINC00470 acts as a positive regulator of AKT activation in GBM.
  • LINC00470 forms a ternary complex with FUS and AKT, stabilizing FUS in the cytoplasm and enhancing AKT activity.
  • Increased AKT activity, driven by LINC00470, suppresses HK1 ubiquitination and cell autophagy, impacting glycolysis.
  • Higher LINC00470 expression correlates with GBM tumorigenesis and poorer patient prognosis.

Conclusions:

  • A novel noncanonical AKT activation pathway involving LINC00470 and FUS in GBM progression is identified.
  • LINC00470 serves as a direct AKT activator, promoting GBM.
  • LINC00470 expression is a significant prognostic indicator for GBM patients.
Keywords:
AKT activationGBMLncRNAOncogene

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