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Nutrient Stress-Dysregulated Antisense lncRNA GLS-AS Impairs GLS-Mediated Metabolism and Represses Pancreatic Cancer

Shi-Jiang Deng1, Heng-Yu Chen1, Zhu Zeng1

  • 1Department of Emergency Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Cancer Research
|December 20, 2018
PubMed

Insights

A novel long noncoding RNA, GLS-AS, regulates pancreatic cancer metabolism by controlling the Myc/GLS pathway. Its downregulation promotes cancer growth, suggesting GLS-AS as a potential therapeutic target for metabolic reprogramming.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Metabolism

Background:

  • Pancreatic cancer cells exhibit metabolic reprogramming, including enhanced glycolysis and glutamine metabolism, to support rapid proliferation and metastasis.
  • The role of long noncoding RNAs (lncRNAs) in coordinating metabolic shifts in pancreatic cancer remains largely undefined.

Purpose of the Study:

  • To identify and characterize the function of lncRNAs involved in pancreatic cancer metabolism.
  • To elucidate the regulatory mechanism of a specific lncRNA, GLS-AS, in pancreatic cancer cell growth and invasion.

Main Methods:

  • Identification of GLS-AS as a nuclear-enriched antisense lncRNA regulating glutaminase (GLS).
  • In vitro and in vivo experiments (xenograft tumors) to assess the impact of GLS-AS depletion on pancreatic cancer cell proliferation and invasion.
  • Investigation of the posttranscriptional regulation of GLS by GLS-AS via RNA interference pathways (ADAR/Dicer).
  • Analysis of the transcriptional regulation of GLS-AS by Myc under nutrient stress and the feedback loop between GLS-AS and Myc stability.

Main Results:

  • GLS-AS was found to be downregulated in pancreatic cancer tissues.
  • Depletion of GLS-AS enhanced pancreatic cancer cell proliferation and invasion.
  • GLS-AS inhibits GLS expression posttranscriptionally and is transcriptionally downregulated by Myc under nutrient stress.
  • A reciprocal feedback loop between Myc and GLS-AS was identified, regulating GLS overexpression during nutrient stress.
  • Ectopic GLS-AS expression suppressed tumor growth by repressing the Myc/GLS pathway.
  • GLS-AS expression inversely correlated with GLS expression in clinical samples, with low GLS-AS associated with poor outcomes.

Conclusions:

  • The study identifies a novel lncRNA, GLS-AS, as a critical regulator of pancreatic cancer metabolism.
  • GLS-AS mediates a feedback loop involving Myc and GLS, impacting cancer cell proliferation and invasion.
  • The lncRNA-mediated Myc/GLS pathway represents a potential therapeutic target for metabolic reprogramming in pancreatic cancer.

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