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This research investigates how METTL3 promotes immune escape in pancreatic cancer by modifying AFAP1-AS1 to affect EGR2 stability.

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February 8, 2026Open Access

METTL3 promotes pancreatic cancer immune escape by m6A modification of lncRNA AFAP1-AS1 to enhance EGR2 stability

Key Points

This research investigates how METTL3 promotes immune escape in pancreatic cancer by modifying AFAP1-AS1 to affect EGR2 stability.
Examined the role of METTL3 in relation to AFAP1-AS1 and EGR2 in pancreatic cancer cells.
Utilized m6A modification analysis to assess stability of lncRNA and mRNA.
Evaluated the impact of EGR2 on immune checkpoint and EMT-related gene transcription.
METTL3 enhances AFAP1-AS1 stability through m6A modification.
Increased EGR2 expression leads to upregulation of immune checkpoint and EMT genes.
The METTL3/AFAP1-AS1/EGR2 axis is implicated in pancreatic cancer malignancy and immune resistance.

Abstract

METTL3 enhances AFAP1-AS1 stability via m6A modification recognized by YTHDF2 and IGF2BP1, which subsequently increases EGR2 expression by improving its mRNA stability. EGR2 directly activates transcription of immune checkpoint and epithelial-mesenchymal transition (EMT)-related genes. This METTL3/AFAP1-AS1/EGR2 signaling axis drives PC malignancy and immune resistance, offering potential therapeutic targets for PC treatment.

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