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Long-term MNNG exposure promotes gastric carcinogenesis by activating METTL3/m6A/miR1184 axis-mediated

Tong Liu1, Yan-Lu Feng2, Rui-Ying Wang3

  • 1Institute of Occupational Health and Environmental Health, School of Public Health, Lanzhou University, Lanzhou, Gansu, PR China; Key Laboratory of Environmental Medicine Engineering, Ministry of Education, School of Public Health, Southeast University, Nanjing, Jiangsu, PR China.

The Science of the Total Environment
|January 1, 2024
PubMed

Insights

N-methyl-N-nitro-N-nitrosoguanidine (MNNG) exposure increases METTL3, a key factor in gastric cancer (GC) development. Targeting METTL3 may offer new treatments for MNNG-induced GC.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • N-methyl-N-nitro-N-nitrosoguanidine (MNNG) is linked to gastric cancer (GC).
  • The precise mechanisms of MNNG-induced GC and the role of METTL3 are not fully understood.

Purpose of the Study:

  • To investigate the clinical significance of METTL3 in GC.
  • To elucidate the role of METTL3 in MNNG-induced gastric carcinogenesis.

Main Methods:

  • Analysis of METTL3 expression in GC patient cohorts.
  • In vitro and in vivo models of MNNG exposure.
  • me-RIP sequencing to identify METTL3-regulated miRNAs.
  • Functional assays assessing cell proliferation, migration, invasion, and tumorigenesis.

Main Results:

  • Long-term MNNG exposure elevated METTL3 and epithelial-mesenchymal transition (EMT) markers.
  • METTL3 depletion inhibited proliferation, migration, invasion, and tumorigenesis in MNNG-transformed and GC cells.
  • METTL3 was found to regulate the miR-1184/TRPM2 axis via miRNA-118.

Conclusions:

  • METTL3 plays a critical role in epigenetic regulation during MNNG-induced gastric carcinogenesis.
  • METTL3 and its associated miR-1184/TRPM2 pathway represent potential therapeutic targets for GC treatment.
Keywords:
EMTMETTL3MNNGm6A modification, gastric cancermiR-1184

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