LncRNA B4GALT 1-AS1/miR-144-3p axis suppresses cytotoxicity of CD8+ T cells in lung adenocarcinoma by modulating

Lifei Huang1, Jiadong Wu1, Yahong Sun1

  • 1Department of Respiratory and Critical Care Medicine, Haining People's Hospital, No. 2 Qianjiang West Road, Haining, 314400, China.

Discover Oncology
|September 26, 2025
PubMed
Abstract

Insights

This study reveals a new mechanism of immune escape in lung adenocarcinoma (LUAD) involving the long non-coding RNA B4GALT1-AS1 and microRNA miR-144-3p. This axis suppresses CD8+ T cell activity, offering potential targets for novel immunotherapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Lung adenocarcinoma (LUAD) has a high mortality rate with limited immunotherapy success.
  • Understanding novel immune escape mechanisms is crucial for LUAD treatment.

Purpose of the Study:

  • To investigate the role of the long non-coding RNA (lncRNA) B4GALT1-AS1 and microRNA (miRNA) miR-144-3p in LUAD immune escape.
  • To elucidate the lncRNA-miRNA network's impact on LUAD progression and T cell response.

Main Methods:

  • Bioinformatics analysis to determine expression and predict binding sites of B4GALT1-AS1 and miR-144-3p.
  • Experimental validation including RNA immunoprecipitation, dual-luciferase, and RNA pull-down assays.
  • Assessment of LUAD cell proliferation, migration, invasion, and CD8+ T cell cytotoxicity in a co-culture system.

Main Results:

  • B4GALT1-AS1 was highly expressed, while miR-144-3p was lowly expressed in LUAD.
  • B4GALT1-AS1 promoted LUAD cell proliferation, migration, invasion, and immune escape by acting as a molecular sponge for miR-144-3p.
  • The B4GALT1-AS1/miR-144-3p axis modulated programmed death-ligand 1 (PD-L1) expression, suppressing CD8+ T cell cytotoxicity.

Conclusions:

  • The B4GALT1-AS1/miR-144-3p axis is a novel immune escape mechanism in LUAD.
  • This axis suppresses CD8+ T cell cytotoxicity by regulating PD-L1 expression.
  • Targeting the B4GALT1-AS1/miR-144-3p axis holds potential for developing new LUAD immunotherapies.

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