ArticleOncoTargets and therapy2020
miR-519d-3p Overexpression Inhibits P38 and PI3K/AKT Pathway via Targeting VEGFA to Attenuate the Malignant Biological Behavior of Non-Small Cell Lung Cancer.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Non-coding RNAs and regulation of the PI3K signaling pathway in lung cancer: Recent insights and potential clinical applications.Non-coding RNA research · 2025Review
- AAAGUGC Seed-Containing miRNAs: Master Regulators of Cancer Pathways and Therapeutic Resistance.MicroRNA (Shariqah, United Arab Emirates) · 2025Review
- Advances in the role of microRNAs associated with the PI3K/AKT signaling pathway in lung cancer.Frontiers in oncology · 2023Review
- Transcription factor p53-mediated activation of miR-519d-3p and downregulation of E2F1 attenuates prostate cancer growth and metastasis.Cancer gene therapy · 2022Article
- Identification and validation of aging-related genes in COPD based on bioinformatics analysis.Aging · 2022Article
- Article
- Notoginsenoside R2 induces colonic microvascular injuries via regulating the Rap1GAP/PI3K/Akt signaling pathway.Annals of translational medicine · 2021Article
- CircMYOF triggers progression and facilitates glycolysis via the VEGFA/PI3K/AKT axis by absorbing miR-4739 in pancreatic ductal adenocarcinoma.Cell death discovery · 2021Article
- The Hypoxia-Long Noncoding RNA Interaction in Solid Cancers.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-small cell lung cancer (NSCLC) is a heterogeneous tumor that accounts for approximately 85% of all lung cancer cases worldwide. microRNAs (miRNAs) are believed to play an important role in regulating a variety of biological processes, including immunity and cancer. We investigated the effect of miR-519d-3p on the mitigation of NSCLC in vitro and in vivo.
methodsRT-PCR or immunohistochemical assays were used to assess the expression of miR-519d-3p. Colony formation, flow cytometry, and transwell assay were respectively used to detect proliferation, apoptosis, and invasion of A549 and NCI-H661 cell lines. Luciferase reporter assay was used to verify targeting the relationship between mir-519d-3p and VEGFA. Western blot was used to examine the expression of Ki67, caspase-3, E-cadherin, N-cadherin, VEGF, P38, and PI3K/AKT. Animal models were established by BABL/c mice to research the effect of mir-519d-3p overexpression in vivo.
resultsIn vitro, miR-519d-3p overexpression inhibited A549 and NCI-H661 cells proliferation, invasion, and also promoted apoptosis. In addition, miR-519d-3p overexpression downregulated VEGFA expression and decreased the P38 and PI3K/AKT phosphorylation level. In vivo, miR-519d-3p overexpression significantly restrained tumor volume (2087±265 mm
conclusionThe data indicated that miR-519d-3p could be a novel therapy or adjuvant against NSCLC.
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