ArticleActa pharmacologica Sinica2022
Promoter methylation-regulated miR-148a-3p inhibits lung adenocarcinoma (LUAD) progression by targeting MAP3K9.
Article in Acta pharmacologica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- A Panel of Circulating Exosomal sncRNAs Associated With Lung Cancer Risk up to 10 Years in Advance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Research progress of MicroRNA in lung cancer.Discover oncology · 2026Review
- MiR-148a-3p/SIRT7 axis promotes glioma progression and regulates temozolomide chemosensitivity.Journal of neuro-oncology · 2025Article
- Aging-related signature stratifies LUAD prognosis and uncovers senescence-induced chemoresistance via NF-κB/RELA activation.Respiratory research · 2025Article
- A microsphere loaded with chondrocyte-targeting exosomes continuously deliver miR-148a for osteoarthritis therapy.Materials today. Bio · 2025Article
- The Role of microRNAs in Lung Cancer: Mechanisms, Diagnostics and Therapeutic Potential.International journal of molecular sciences · 2025Review
- Improved Predictability of Diagnosis and Prognosis Using Serum- and Tissue-Derived Extracellular Vesicles From Bulk mRNA Sequencing in Pancreatic Ductal Adenocarcinoma.Cancer medicine · 2025Article
- MiRNAs and Microbiota in Non-Small Cell Lung Cancer (NSCLC): Implications in Pathogenesis and Potential Role in Predicting Response to ICI Treatment.International journal of molecular sciences · 2024Review
- Review
- LncRNA SLC16A1-AS1 participates in the initiation and progression of colorectal cancer by regulating MAP3K9 expression through targeting miR-515-5p.American journal of cancer research · 2024Article
- Targeting Reprogrammed Cancer-Associated Fibroblasts with Engineered Mesenchymal Stem Cell Extracellular Vesicles for Pancreatic Cancer Treatment.Biomaterials research · 2024Article
- Article
- Review
- Article
- Inhibition of YAP1 activity ameliorates acute lung injury through promotion of M2 macrophage polarization.MedComm · 2023Article
- The Importance of the Immune System and Molecular Cell Signaling Pathways in the Pathogenesis and Progression of Lung Cancer.International journal of molecular sciences · 2023Review
- The reversion of DNA methylation-induced miRNA silence via biomimetic nanoparticles-mediated gene delivery for efficient lung adenocarcinoma therapy.Molecular cancer · 2022Article
- Identification and comprehensive analysis of circRNA-miRNA-mRNA regulatory networks in osteoarthritis.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung adenocarcinoma (LUAD) characterized by high metastasis and mortality is the leading subtype of non-small cell lung cancer. Evidence shows that some microRNAs (miRNAs) may act as oncogenes or tumor suppressor genes, leading to malignant tumor occurrence and progression. To better understand the molecular mechanism associated with miRNA methylation in LUAD progression and clinical outcomes, we investigated the correlation between miR-148a-3p methylation and the clinical features of LUAD. In the LUAD cell lines and tumor tissues from patients, miR-148a-3p was found to be significantly downregulated, while the methylation of miR-148a-3p promoter was notably increased. Importantly, miR-148a-3p hypermethylation was closely associated with lymph node metastasis. We demonstrated that mitogen-activated protein (MAP) kinase kinase kinase 9 (MAP3K9) was the target of miR-148a-3p and that MAP3K9 levels were significantly increased in both LUAD cell lines and clinical tumor tissues. In A549 and NCI-H1299 cells, overexpression of miR-148a-3p or silencing MAP3K9 significantly inhibited cell growth, migration, invasion and cytoskeleton reorganization accompanied by suppressing the epithelial-mesenchymal transition. In a nude mouse xenograft assay we found that tumor growth was effectively inhibited by miR-148a-3p overexpression. Taken together, the promoter methylation-associated decrease in miR-148a-3p could lead to lung cancer metastasis by targeting MAP3K9. This study suggests that miR-148a-3p and MAP3K9 may act as novel therapeutic targets for the treatment of LUAD and have potential clinical applications.
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