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lncRNA GAS6-AS1 inhibits progression and glucose metabolism reprogramming in LUAD via repressing E2F1-mediated

Jing Luo1,2, Huishan Wang3, Li Wang4

  • 1Department of Thoracic Surgery, The Affiliated Cancer Hospital of Nanjing Medical University & Jiangsu Cancer Hospital & Jiangsu Institute of Cancer Research, Jiangsu Key Laboratory of Molecular and Translational Cancer Research, Nanjing 210000, China.

Molecular Therapy. Nucleic Acids
|June 18, 2021
PubMed

Insights

Long noncoding RNA GAS6-AS1 suppresses lung adenocarcinoma (LUAD) progression by inhibiting glucose metabolism. GAS6-AS1 acts as a tumor suppressor, potentially serving as a therapeutic target for LUAD.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metabolism

Background:

  • Glucose metabolism reprogramming is a hallmark of cancer.
  • The role of long noncoding RNAs (lncRNAs) in lung adenocarcinoma (LUAD) glucose metabolism is not fully understood.

Purpose of the Study:

  • To investigate the function of GAS6-AS1 in LUAD progression and glucose metabolism.
  • To elucidate the molecular mechanisms underlying GAS6-AS1's role in LUAD.

Main Methods:

  • In vitro and in vivo experiments to assess tumor progression.
  • Metabolism-related assays to analyze glucose metabolism.
  • Western blotting and qRT-PCR to examine gene expression.
  • RNA immunoprecipitation and luciferase reporter assays to determine molecular interactions.

Main Results:

  • Overexpression of GAS6-AS1 suppressed LUAD progression and inhibited glucose metabolism.
  • GAS6-AS1 repressed GLUT1 expression by interacting with E2F1, suppressing GLUT1 transcription.
  • GAS6-AS1 was downregulated in LUAD tissues and correlated with poor prognosis.

Conclusions:

  • GAS6-AS1 acts as a tumor suppressor in LUAD by inhibiting glucose metabolism reprogramming.
  • GAS6-AS1 may serve as a prognostic biomarker and therapeutic target for LUAD.
Keywords:
E2F1GAS6-AS1GLUT1glucose metabolismlung adenocarcinoma

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