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MiR-652-5p elevated glycolysis level by targeting TIGAR in T-cell acute lymphoblastic leukemia

Shan Liu1,2,3,4, Haobiao Wang1,2,3,4, Wei Guo5

  • 1Center for Clinical Molecular Laboratory Medicine/Newborn Screening Center of Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.

Cell Death & Disease
|February 15, 2022
PubMed

Insights

Impaired miR-652-5p slows acute T lymphoblastic leukemia (T-ALL) growth by repressing glycolysis. This microRNA targets Tigar, a key regulator of glycolysis, offering a potential therapeutic target for T-ALL.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Biochemistry

Background:

  • Glycolysis plays a role in acute T lymphoblastic leukemia (T-ALL), but its precise mechanisms are unclear.
  • MicroRNA (miRNA) dysregulation is implicated in cancer glycolysis by targeting rate-limiting enzymes.
  • Previous work identified miR-223 targeting miR-652-5p in T-ALL.

Purpose of the Study:

  • To investigate the role of miR-652-5p in T-ALL progression and glycolysis.
  • To elucidate the molecular mechanisms underlying miR-652-5p's function in T-ALL.
  • To evaluate miR-652-5p as a potential therapeutic target for T-ALL.

Main Methods:

  • Assessed the impact of miR-652-5p expression on T-ALL cell growth, apoptosis, and survival in vitro and in vivo.
  • Utilized Gene Ontology (GO) enrichment analysis to identify miR-652-5p targets.
  • Measured glycolysis-related metabolites (lactate, pyruvate, ATP) and metabolic rates (ECAR, OCR).
  • Performed molecular experiments to confirm the interaction between miR-652-5p, Tigar, and PFKFB3.

Main Results:

  • Reduced miR-652-5p expression inhibited T-ALL cell growth, promoted apoptosis, and improved survival.
  • Impaired miR-652-5p led to decreased glycolysis (lower lactate, pyruvate, ATP, ECAR) and increased respiration (higher OCR).
  • miR-652-5p directly targets Tigar mRNA, inhibiting its expression; Tigar, in turn, suppresses the glycolysis enzyme PFKFB3.

Conclusions:

  • The miR-652-5p/Tigar axis plays a crucial role in regulating glycolysis in T-ALL.
  • Downregulation of miR-652-5p represses glycolysis, thereby inhibiting T-ALL cell growth.
  • miR-652-5p represents a promising novel therapeutic target for T-ALL treatment.

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