ArticleFrontiers in cellular neuroscience2016
Low-Dose Endothelial-Monocyte-Activating Polypeptide-II Induced Autophagy by Down-Regulating miR-20a in U-87 and U-251 Glioma Cells.
Article in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- AIMP1: multifunctional regulator in physiology and pathology with therapeutic implications.PeerJ · 2025Review
- Expression and significant roles of the long non-coding RNA CASC19/miR-491-5p/HMGA2 axis in the development of gastric cancer.World journal of gastrointestinal oncology · 2024Article
- Insights on E1-like enzyme ATG7: functional regulation and relationships with aging-related diseases.Communications biology · 2024Review
- Review
- EMAP II Expression Is Increased on Peripheral Blood Cells from Non-Hodgkin Lymphoma.Journal of immunology research · 2022Article
- Cytotoxic Effects of Arsenite in Combination With Gamabufotalin Against Human Glioblastoma Cell Lines.Frontiers in oncology · 2021Article
- Roles of aminoacyl-tRNA synthetase-interacting multi-functional proteins in physiology and cancer.Cell death & disease · 2020Review
- Advances in circular RNAs and their role in glioma (Review).International journal of oncology · 2020Article
- Mechanical stimulation of Schwann cells promote peripheral nerve regeneration via extracellular vesicle-mediated transfer of microRNA 23b-3p.Theranostics · 2020Article
- Mir-26b inhibits growth and resistance to paclitaxel chemotherapy by silencing the CDC6 gene in gastric cancer.Archives of medical science : AMS · 2019Article
- Endothelial Monocyte-Activating Polypeptide-II Induces BNIP3-Mediated Mitophagy to Enhance Temozolomide Cytotoxicity of Glioma Stem Cells via Down-Regulating MiR-24-3p.Frontiers in molecular neuroscience · 2018Article
- Combination of Endothelial-Monocyte-Activating Polypeptide-II with Temozolomide Suppress Malignant Biological Behaviors of Human Glioblastoma Stem Cells via miR-590-3p/MACC1 Inhibiting PI3K/AKT/mTOR Signal Pathway.Frontiers in molecular neuroscience · 2017Article
- The Role of miR-330-3p/PKC-α Signaling Pathway in Low-Dose Endothelial-Monocyte Activating Polypeptide-II Increasing the Permeability of Blood-Tumor Barrier.Frontiers in cellular neuroscience · 2017Article
- Endothelial-Monocyte Activating Polypeptide II Suppresses theFrontiers in molecular neuroscience · 2017Article
- microRNA-20a Inhibits Autophagic Process by Targeting ATG7 and ATG16L1 and Favors Mycobacterial Survival in Macrophage Cells.Frontiers in cellular and infection microbiology · 2016Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Preliminary studies have shown that endothelial-monocyte-activating polypeptide-II (EMAP-II) induces autophagy and inhibits the viability of glioma cells via an unknown molecular mechanism. This study explored the possible mechanisms associated with EMAP-II-induced autophagy in glioma cells by regulation of the expression of microRNA-20a (miR-20a). EMAP-II effectively inhibited the viability, migration and invasion of human U-87 and U-251 glioma cells. EMAP-II also up-regulated the expression level of autophagy biomarker microtubule-associated protein one light chain 3 (LC3)-II/I, autophagy related gene ATG7 and ATG5, but down-regulated autophagy substrate P62/SQSTM1 protein expression. The expression levels of miR-20a decreased significantly after U-87 and U-251 cells were treated with EMAP-II. MiR-20a overexpression partly reversed the EMAP-II-induced up-regulation of LC3-II/I and down-regulation of P62/SQSTM1. MiR-20a had a negative regulatory effect on the expression of the proteins ATG7 and ATG5; which were also targets of miR-20a, as detected by a dual-luciferase reporter assay. In addition, both EMAP-II and miR-20a inhibition significantly reduced the viability, migration and invasion of U-87 and U-251 cells, and their combination showed a synergistic effect. Furthermore, nude mice carrying silencing-expressed miR-20a combined with EMAP-II treatment produced the smallest tumors and the highest survival. In summary, low-dose EMAP-II increased expression levels of ATG5 and ATG7 via down-regulation of the expression of miR-20a. This activated the autophagy pathway, thereby significantly inhibiting the viability, migration and invasion of U-87 and U-251 glioma cells. The combined treatment of EMAP-II with a miR-20a inhibitor showed a synergistic effect against glioma.
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