ArticleThoracic cancer2023
EIF4A3 stabilizes the expression of lncRNA AGAP2-AS1 to activate cancer-associated fibroblasts via MyD88/NF-κb signaling.
Article in Thoracic cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Exosomal lncRNA PVT1 promotes fibroblast activation and colon cancer progression via miR-23b-5p signaling.The Journal of pathology · 2026Article
- CircRSF1 Promoted HepG2 Cell Proliferation, Migration and Invasion Depending on EIF4A3.Digestive diseases and sciences · 2026Article
- Emerging agents that target signaling pathways in cancer fibroblast cells (Review).International journal of oncology · 2026Review
- The DIAPH3/RPL6 axis regulates the cGAS-STING pathway in pancreatic cancer.European journal of medical research · 2025Article
- Exosomes promote pre-metastatic niche formation in lung cancer.Cancer cell international · 2025Review
- DEAD-box RNA helicases in the multistep process of tumor metastasis.Molecular biology reports · 2024Review
- Long Non-Coding RNAMolecules (Basel, Switzerland) · 2024Review
- Identification of Novel Prognostic Long Non-coding RNAs in Lung Adenocarcinoma Using WGCNA Analysis.Biochemical genetics · 2024Article
- Long non-coding RNAs are involved in the crosstalk between cancer-associated fibroblasts and tumor cells.Frontiers in immunology · 2024Review
- Crosstalk with lung fibroblasts shapes the growth and therapeutic response of mesothelioma cells.Cell death & disease · 2023Article
- EIF4A3 stabilizes the expression of lncRNA AGAP2-AS1 to activate cancer-associated fibroblasts via MyD88/NF-κb signaling.Thoracic cancer · 2023Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLung cancer (LC) is a fatal malignancy and often accompanied with converting normal fibroblasts to cancer-associated fibroblasts (CAFs). Exosomal lncRNA AGAP2-AS1 has been elucidated to be a potent prognostic factor for LC, while its role in activating CAFs is largely unknown.
methodsWe first extracted exosomes from LC patients and co-cultured them with MRC5 cells to observe the state of MRC5 cells, detect AGAP2-AS1 using real-time quantitative polymerase chain reaction, and then analyze the interaction between EIF4A3 and AGAP2-AS1 using RNA pull down experiments. CCK-8 assay was used to detect cell proliferation. Transwell experiments demonstrated the regulation of MRC5 cells and, finally, the role of MyD88/NF-κB in the downstream mechanism of EIF4A3/AGAP2-AS1 was explored by RNA interference technology and pyrrolidinedithiocarbamic acid inhibition.
resultsWe demonstrated that exosomes from the LC patients (cancer-exo) notably increased the metastatic ability of MRC-5 cells, promoting the expressions of the CAF biomarkers and lncRNA AGAP2-AS1. Overexpression of lncRNA AGAP2-AS1 prominently activated MRC-5 cells. Moreover, EIF4A3 was upregulated in the cancer-exo-treated MRC-5 cells, and EIF4A3 was verified to bind with lncRNA AGAP2-AS1 to improve its stability. The MyD88/NF-κB signaling pathway was subsequently proved to be positively regulated by lncRNA AGAP2-AS1, and the promotive role of lncRNA AGAP2-AS1 in LC and activating CAFs was confirmed in vivo.
conclusionsThe positive feedback of EIF4A3/AGAP2-AS1/MyD88/NF-κB signaling pathway contributed to the activation of CAFs and exacerbated LC in turn, revealing a novel regulatory axis underlying LC.
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