ArticleJournal of translational medicine2022
MIR99AHG inhibits EMT in pulmonary fibrosis via the miR-136-5p/USP4/ACE2 axis.
Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Naringin nanoparticles alleviate RA-ILD pulmonary fibrosis by targeting 14-3-3ζ to inhibit LYVE1Materials today. Bio · 2026Article
- Vitamin D receptor suppresses pulmonary fibroblast activation by downregulating the TGF-β1/Smad signaling pathway.Histochemistry and cell biology · 2026Article
- Clinical Significance and Potential Molecular Mechanisms of Angiotensin-Converting Enzyme 2 in Colorectal Cancer.World journal of oncology · 2026Article
- Decoding the lncRNA-miRNA-mRNA network in sepsis-induced lung injury: from pathogenesis to extracellular vesicle-based therapy.Frontiers in immunology · 2026Review
- LncRNA MIR99AHG serves as a diagnostic marker for early lung cancer and regulates cancer cell growth and metastasis via miR-194-5p.Discover oncology · 2025Article
- LncRNA SYISL promotes fibroblast myofibroblast transition via miR-23a-mediated TRIOBP regulation.Cellular and molecular life sciences : CMLS · 2025Article
- Exploring the mitigating potential of anthocyanin Malvidin in a mouse model of bleomycin-induced pulmonary fibrosis by inhibiting NLRP3 inflammasome activation and oxidative stress.Journal of inflammation (London, England) · 2025Article
- Article
- The role of the classical renin-angiotensin system and angiotensin-converting enzyme 2/Ang(1-7)/Mas axis in pulmonary fibrosis.Frontiers in medicine · 2025Review
- Molecular Mechanisms and Roles of MiR-136-5p in Human Cancer and Other Disorders.Current medicinal chemistry · 2025Review
- Pathogenesis and Therapy of Hermansky-Pudlak Syndrome (HPS)-Associated Pulmonary Fibrosis.International journal of molecular sciences · 2024Review
- Assessing the impact of triiodothyronine treatment on the lung microbiome of mice with pulmonary fibrosis.BMC pulmonary medicine · 2024Article
- Epigenetic Regulation of EMP/EMT-Dependent Fibrosis.International journal of molecular sciences · 2024Review
- Article
- Crosstalk of ubiquitin system and non-coding RNA in fibrosis.International journal of biological sciences · 2024Review
- LncRNA PRKCA-AS1 promotes LUAD progression and function as a ceRNA to regulate S100A16 by sponging miR-508-5p.Journal of Cancer · 2024Article
- ACE2: the node connecting the lung cancer and COVID-19.American journal of cancer research · 2024Review
- Differential expression and clinical significance of long non-coding RNAs in the development and progression of lung adenocarcinoma.Frontiers in oncology · 2024Review
- ACE2 in chronic disease and COVID-19: gene regulation and post-translational modification.Journal of biomedical science · 2023Review
- LINC01117 inhibits invasion and migration of lung adenocarcinoma through influencing EMT process.PloS one · 2023Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLong non-coding RNAs (lncRNAs) are closely related to the occurrence and development of cancer. Abnormally expressed lncRNA can be used as a diagnostic marker for cancer. In this study, we aim to investigate the clinical significance of MIR99AHG expression in lung adenocarcinoma (LUAD), and its biological roles in LUAD progression.
methodsThe relative expression of MIR99AHG in LUAD tissues and cell lines was analyzed using public databases and RT-qPCR. The biological functions of MIR99AHG were investigated using a loss-of-function approach. The effect of MIR99AHG on lung fibrosis was assessed by scratch assay, invasion assay and lung fibrosis rat model. FISH, luciferase reporter assay and immunofluorescence were performed to elucidate the underlying molecular mechanisms.
resultsLncRNA MIR99AHG expression level was downregulated in LUAD tissues and cell lines. Low MIR99AHG levels were associated with poorer patient overall survival. Functional analysis showed that MIR99AHG is associated with the LUAD malignant phenotype in vitro and in vivo. Further mechanistic studies showed that, MIR99AHG functions as a competitive endogenous RNA (ceRNA) to antagonize miR-136-5p-mediated ubiquitin specific protease 4 (USP4) degradation, thereby unregulated the expression of angiotensin-converting enzyme 2 (ACE2), a downstream target gene of USP4, which in turn affected alveolar type II epithelial cell fibrosis and epithelial-mesenchymal transition (EMT). In summary, the MIR99AHG/miR-136-5p/USP4/ACE2 signalling axis regulates lung fibrosis and EMT, thus inhibiting LUAD progression.
conclusionThis study showed that downregulated MIR99AHG leads to the development of pulmonary fibrosis. Therefore, overexpression of MIR99AHG may provide a new approach to preventing LUAD progression.
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