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Modulating redox homeostasis and cellular reprogramming through inhibited methylenetetrahydrofolate dehydrogenase 2

Chun-Hao Chan1,2, Chia-Yu Wu3,4, Navneet Kumar Dubey1,2

  • 1School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei 11031, Taiwan.

Aging
|August 8, 2020
PubMed

Insights

Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) drives lung cancer growth and aggressiveness. Inhibiting MTHFD2 significantly reduces cancer cell viability, self-renewal, and tumor formation, offering a potential therapeutic target.

Area of Science:

  • Biochemistry
  • Oncology
  • Molecular Biology

Background:

  • Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) is increasingly linked to poor cancer survival.
  • The precise metabolic functions and cellular reprogramming roles of MTHFD2 in lung cancer remain incompletely understood.

Purpose of the Study:

  • To investigate the metabolic functions of MTHFD2 in lung cancer (LCa).
  • To assess the impact of MTHFD2 on cellular reprogramming and tumorigenicity in LCa.

Main Methods:

  • Confirmed MTHFD2 expression in LCa tissues and cell lines (A549, H1299, H441) using Oncomine™ database and molecular analysis.
  • Utilized lentiviral transduction for MTHFD2 gene knockdown to reprogram metabolic activities.
  • Assessed cellular viability, transformation, self-renewal, and in vivo tumorigenicity in NOD/SCID mice.

Main Results:

  • MTHFD2 expression was significantly elevated in a stage-dependent manner in LCa tissues and cell lines.
  • MTHFD2 knockdown markedly inhibited LCa cell viability, transformation, and self-renewal.
  • Tumorigenicity assays demonstrated suppressed tumor initiation and reduced tumor size in MTHFD2-knockdown groups.
  • Low oxygen tension assays indicated that MTHFD2 knockdown suppressed stemness and sphere formation.

Conclusions:

  • MTHFD2 plays a critical role in metabolic reprogramming essential for lung cancer cell growth and aggressiveness.
  • Suppression of MTHFD2 effectively inhibits LCa progression and tumor aggressiveness, highlighting its potential as a therapeutic target.
Keywords:
MTHFD2lung canceroxygen tensiontumorigenicity

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