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m6A-modified circZNF548 regulates exosomal miR-7108-3p to activate CD3+CD8+ T cells and suppress NSCLC growth by JMY

Yu-Long Zhao1,2, You-Jie Li1, Chun-Xia Wu1

  • 1Department of Biochemistry and Molecular Biology, Binzhou Medical University, YanTai, Shandong, 264003, People's Republic of China.

BMC Biology
|August 15, 2025
PubMed
Abstract

Insights

N6-methyladenosine (m6A)-modified circZNF548 suppresses non-small cell lung cancer (NSCLC) growth and spread. It enhances anti-tumor immunity by regulating exosomal miR-7108-3p and the JMY-p53 pathway, offering potential new NSCLC therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Tumor microenvironment (TME) communication influences cancer malignancy.
  • Circular RNAs (circRNAs) are stable molecules involved in TME remodeling.
  • N6-methyladenosine (m6A) modification impacts gene expression and cancer progression.

Purpose of the Study:

  • Investigate the role of m6A-modified circZNF548 in non-small cell lung cancer (NSCLC).
  • Determine circZNF548's influence on NSCLC proliferation, migration, and the TME.
  • Elucidate the molecular mechanisms involving circZNF548, m6A modification, and immune response in NSCLC.

Main Methods:

  • Quantitative analysis of circZNF548 expression in NSCLC tissues and adjacent normal tissues.
  • Overexpression and siRNA-mediated knockdown of circZNF548 and METTL14 to assess proliferation and migration.
  • Interaction studies between circZNF548 and exosomal miR-7108-3p.
  • Analysis of downstream targets of miR-7108-3p (CD8A, JMY) and their pathways.
  • Assessment of T cell activation markers (CD107a, IFN-γ, perforin 1, granzyme B) in the TME.

Main Results:

  • circZNF548 expression is downregulated in NSCLC, correlating with poorer survival.
  • circZNF548 overexpression inhibits NSCLC proliferation and migration; knockdown promotes them.
  • METTL14 regulates circZNF548 levels via m6A modification.
  • circZNF548 modulates exosomal miR-7108-3p, which targets CD8A and JMY.
  • Exosomal miR-7108-3p suppresses CD3+CD8+ T cell activation, while circZNF548 enhances T cell-mediated cytotoxicity via miR-7108-3p and the JMY-p53 pathway.

Conclusions:

  • m6A-modified circZNF548 suppresses NSCLC progression by enhancing anti-tumor immunity.
  • The mechanism involves modulation of exosomal miR-7108-3p and the JMY-p53 pathway.
  • circZNF548 represents a potential therapeutic target for NSCLC treatment.
Keywords:
CD8Exosomal miR-7108-3pJMYTumor microenvironmentcircZNF548

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