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Updated: Jan 16, 2026

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
Published on: March 30, 2019
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.
Background:
For lung adenocarcinoma (LUAD), which has the highest mortality rate among cancers, the current known immunotherapy has only achieved limited results. This article aimed to clarify the novel immune escape mechanism in LUAD based on the long non-coding RNA (lncRNA)-microRNA (miRNA) network.
Methods:
By bioinformatics analysis, the expression of B4GALT1-AS1 and miR-144-3p was determined and the binding sites were predicted. RNA immunoprecipitation assay, dual-luciferase assay, and RNA pull-down experiment were employed to validate their binding. Quantitative reverse transcription polymerase chain reaction was utilized to measure the expression levels. LUAD cell proliferation and cell cycle progression were detected by Colony formation assay and cell cycle analysis. Cell migration and invasion were detected by Transwell assay. A co-culture system evaluated the proportion of IFN-γ positive CD8+ T cells, the cytotoxicity of CD8+ T cells, and cytokines secretion. The expression of programmed death-ligand 1 (PD-L1) was detected by western blot.
Results:
In LUAD, B4GALT1-AS1 was highly expressed, while miR-144-3p was lowly expressed. B4GALT1-AS1 facilitated LC cell proliferation, migration, invasion, inhibited CD8+ T cell toxicity, and promoted immune escape. Furthermore, B4GALT1-AS1 functioned as a molecular sponge for miR-144-3p. Rescue experiments revealed that overexpression of B4GALT1-AS1 up-regulated the expression of PD-L1, and overexpression of miR-144-3p partially attenuated the promoting impact of B4GALT1-AS1 overexpression on LUAD cell proliferation, migration, invasion, and immune escape.
Conclusion:
This study demonstrated that the B4GALT1-AS1/miR-144-3p axis suppressed the cytotoxicity of CD8+ T cells in LUAD by modulating the expression of PD-L1, which will assist in innovating new immunotherapies.
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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