ArticleTechnology in cancer research & treatment
Loading MicroRNA-376c in Extracellular Vesicles Inhibits Properties of Non-Small Cell Lung Cancer Cells by Targeting YTHDF1.
Article in Technology in cancer research & treatment. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Targeting intracellular mRNA mJournal of advanced research · 2026Review
- mActa pharmaceutica Sinica. B · 2025Review
- Recent Advances in the Mutual Regulation of m6A Modification and Non-Coding RNAs in Atherosclerosis.International journal of general medicine · 2025Review
- The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024Review
- The YTH domain-containing protein family: Emerging players in immunomodulation and tumour immunotherapy targets.Clinical and translational medicine · 2024Review
- Readers of RNA Modification in Cancer and Their Anticancer Inhibitors.Biomolecules · 2024Review
- RNA mMolecular oncology · 2023Review
- The potential role of m6A reader YTHDF1 as diagnostic biomarker and the signaling pathways in tumorigenesis and metastasis in pan-cancer.Cell death discovery · 2023Review
- The function and clinical implication of YTHDF1 in the human system development and cancer.Biomarker research · 2023Review
- Effects of writers, erasers and readers within miRNA-related m6A modification in cancers.Cell proliferation · 2023Review
- Emerging Mutual Regulatory Roles between mInternational journal of molecular sciences · 2023Review
- N6-methyladenosine reader YTHDF family in biological processes: Structures, roles, and mechanisms.Frontiers in immunology · 2023Review
- Role of m6A writers, erasers and readers in cancer.Experimental hematology & oncology · 2022Review
- Wnt signaling in colorectal cancer: pathogenic role and therapeutic target.Molecular cancer · 2022Review
- Insight into the structure, physiological function, and role in cancer of m6A readers-YTH domain-containing proteins.Cell death discovery · 2022Review
- Implications of m6A methylation and microbiota interaction in non-small cell lung cancer: From basics to therapeutics.Frontiers in cellular and infection microbiology · 2022Review
- Molecular subtype identification and predictive power of N6-methyladenosine regulator in unexplained recurrent pregnancy loss.Frontiers in genetics · 2022Article
- RBM8A Depletion Decreases the Cisplatin Resistance and Represses the Proliferation and Metastasis of Breast Cancer Cells via AKT/mTOR Pathway.The breast journal · 2022Article
- The roles and mechanisms of the m6A reader protein YTHDF1 in tumor biology and human diseases.Molecular therapy. Nucleic acids · 2021Review
- Knockdown of METTL14 suppresses the malignant progression of non-small cell lung cancer by reducing Twist expression.Oncology letters · 2021Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveExtracellular vesicles (Evs) secreted from cells have been revealed to mediate signal transduction between cells. Nevertheless, the mechanisms through which molecules transported by EVs function remain to be elucidated. In the present study, the functional relevance of endothelial cells (ECs)-secreted Evs carrying microRNA-376c (miR-376c) in the biological activities of non-small cell lung cancer (NSCLC) cells was investigated, including the related mechanisms.
methodsTwo cell lines with the highest YTH N6-methyladenosine (m6A) RNA binding protein 1 (YTHDF1) expression were selected for subsequent experiments. Cellular proliferation, migration, invasion and apoptosis were measured by EdU, wound healing, Transwell assays and flow cytometry, respectively. The binding relationship between miR-376c and YTHDF1 was analyzed by dual-luciferase reporter assays. The miR-376c, YTHDF1 and β-catenin expression was evaluated by qPCR assays and western blot assays.
resultsThe expression patterns of YTHDF1 were higher in NSCLC cells, whereas miR-376c was reduced versus the normal bronchial epithelial cells. Silencing of YTHDF1 repressed NSCLC cell proliferation, invasion and migration abilities, whereas enhanced apoptosis. miR-376c negatively modulated YTHDF1 expression. Under co-culture conditions, ECs transmitted miR-376c into NSCLC cells through Evs, and inhibited the intracellular YTHDF1 expression and the Wnt/β-catenin pathway activation. Rescue experiments revealed that YTHDF1 overexpression reversed the inhibitory role of miR-376c released by EC-Evs in NSCLC cells.
conclusionEC-delivered Evs inhibit YTHDF1 expression and the Wnt/β-catenin pathway induction via miR-376c overexpression, thus inhibiting the malignant phenotypes of NSCLC cells.
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