MicroRNA-218 inhibits the malignant phenotypes of glioma by modulating the TNC/AKT/AP-1/TGFβ1 feedback signaling loop
Gliomas are the most malignant and common tumors of the human brain, and the prognosis of glioma patients is extremely poor MicroRNAs (miRNAs or miRs) play critical roles in different types of cancer by performing post-transcriptional regulation of gene expression Although miR-218 has been demonstra...
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| Veröffentlicht in: | International journal of molecular medicine Jg. 48; H. 5 |
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D.A. Spandidos
01.11.2021
Spandidos Publications UK Ltd |
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| Abstract | Gliomas are the most malignant and common tumors of the human brain, and the prognosis of glioma patients is extremely poor MicroRNAs (miRNAs or miRs) play critical roles in different types of cancer by performing post-transcriptional regulation of gene expression Although miR-218 has been demonstrated to be decreased in gliomas, its role in gliomas remains largely unknown miR-218 expression was analyzed in gliomas and normal brain tissues (control subjects) using a dataset from The Cancer Genome Atlas A series of in vitro and in vivo studies were performed to determine the biological roles of miR-218 in glioma cells Potential targets of miR-218 were identified using a dual-luciferase reporter system Western blot and dual-luciferase reporter system experiments were performed to evaluate the regulatory effect of miR-218 on the tenascin C (TNC)/AKT/activator protein 1 (AP-1)/transforming growth factor β1 (TGFβ1) pathway It was demonstrated that miR-218 was significantly downregulated in gliomas compared with control subjects, and played potent tumor suppressor roles in glioma cells by inhibiting cell proliferation, colony formation, migration, invasion and tumorigenic potential in nude mice, as well as inducing cell cycle arrest and apoptosis Mechanistically, miR-218 inhibited malignant phenotypes of glioma cells by binding to the 3′-untranslated region of its target TNC and subsequently suppressing its expression As a result, miR-218 could reduce AKT phosphorylation and subsequently inhibit transcriptional activity of AP-1 by reducing JNK phosphorylation, downregulating the expression of TGFβ1, while TGFβ1 was able to, in turn, activate the TNC/AKT/AP-1 signaling axis Our data revealed a previously unknown tumor suppressor role of miR-218 by blocking the TNC/AKT/AP-1/TGFβ1-positive feedback loop in glioma |
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| AbstractList | Gliomas are the most malignant and common tumors of the human brain, and the prognosis of glioma patients is extremely poor MicroRNAs (miRNAs or miRs) play critical roles in different types of cancer by performing post-transcriptional regulation of gene expression Although miR-218 has been demonstrated to be decreased in gliomas, its role in gliomas remains largely unknown miR-218 expression was analyzed in gliomas and normal brain tissues (control subjects) using a dataset from The Cancer Genome Atlas A series of in vitro and in vivo studies were performed to determine the biological roles of miR-218 in glioma cells Potential targets of miR-218 were identified using a dual-luciferase reporter system Western blot and dual-luciferase reporter system experiments were performed to evaluate the regulatory effect of miR-218 on the tenascin C (TNC)/AKT/activator protein 1 (AP-1)/transforming growth factor β1 (TGFβ1) pathway It was demonstrated that miR-218 was significantly downregulated in gliomas compared with control subjects, and played potent tumor suppressor roles in glioma cells by inhibiting cell proliferation, colony formation, migration, invasion and tumorigenic potential in nude mice, as well as inducing cell cycle arrest and apoptosis Mechanistically, miR-218 inhibited malignant phenotypes of glioma cells by binding to the 3′-untranslated region of its target TNC and subsequently suppressing its expression As a result, miR-218 could reduce AKT phosphorylation and subsequently inhibit transcriptional activity of AP-1 by reducing JNK phosphorylation, downregulating the expression of TGFβ1, while TGFβ1 was able to, in turn, activate the TNC/AKT/AP-1 signaling axis Our data revealed a previously unknown tumor suppressor role of miR-218 by blocking the TNC/AKT/AP-1/TGFβ1-positive feedback loop in glioma Gliomas are the most malignant and common tumors of the human brain, and the prognosis of glioma patients is extremely poor. MicroRNAs (miRNAs or miRs) play critical roles in different types of cancer by performing post‑transcriptional regulation of gene expression. Although miR‑218 has been demonstrated to be decreased in gliomas, its role in gliomas remains largely unknown. miR‑218 expression was analyzed in gliomas and normal brain tissues (control subjects) using a dataset from The Cancer Genome Atlas. A series of in vitro and in vivo studies were performed to determine the biological roles of miR‑218 in glioma cells. Potential targets of miR‑218 were identified using a dual‑luciferase reporter system. Western blot and dual‑luciferase reporter system experiments were performed to evaluate the regulatory effect of miR‑218 on the tenascin C (TNC)/AKT/activator protein 1 (AP‑1)/transforming growth factor β1 (TGFβ1) pathway. It was demonstrated that miR‑218 was significantly downregulated in gliomas compared with control subjects, and played potent tumor suppressor roles in glioma cells by inhibiting cell proliferation, colony formation, migration, invasion and tumorigenic potential in nude mice, as well as inducing cell cycle arrest and apoptosis. Mechanistically, miR‑218 inhibited malignant phenotypes of glioma cells by binding to the 3'‑untranslated region of its target TNC and subsequently suppressing its expression. As a result, miR‑218 could reduce AKT phosphorylation and subsequently inhibit transcriptional activity of AP‑1 by reducing JNK phosphorylation, downregulating the expression of TGFβ1, while TGFβ1 was able to, in turn, activate the TNC/AKT/AP‑1 signaling axis. Our data revealed a previously unknown tumor suppressor role of miR‑218 by blocking the TNC/AKT/AP‑1/TGFβ1‑positive feedback loop in glioma.Gliomas are the most malignant and common tumors of the human brain, and the prognosis of glioma patients is extremely poor. MicroRNAs (miRNAs or miRs) play critical roles in different types of cancer by performing post‑transcriptional regulation of gene expression. Although miR‑218 has been demonstrated to be decreased in gliomas, its role in gliomas remains largely unknown. miR‑218 expression was analyzed in gliomas and normal brain tissues (control subjects) using a dataset from The Cancer Genome Atlas. A series of in vitro and in vivo studies were performed to determine the biological roles of miR‑218 in glioma cells. Potential targets of miR‑218 were identified using a dual‑luciferase reporter system. Western blot and dual‑luciferase reporter system experiments were performed to evaluate the regulatory effect of miR‑218 on the tenascin C (TNC)/AKT/activator protein 1 (AP‑1)/transforming growth factor β1 (TGFβ1) pathway. It was demonstrated that miR‑218 was significantly downregulated in gliomas compared with control subjects, and played potent tumor suppressor roles in glioma cells by inhibiting cell proliferation, colony formation, migration, invasion and tumorigenic potential in nude mice, as well as inducing cell cycle arrest and apoptosis. Mechanistically, miR‑218 inhibited malignant phenotypes of glioma cells by binding to the 3'‑untranslated region of its target TNC and subsequently suppressing its expression. As a result, miR‑218 could reduce AKT phosphorylation and subsequently inhibit transcriptional activity of AP‑1 by reducing JNK phosphorylation, downregulating the expression of TGFβ1, while TGFβ1 was able to, in turn, activate the TNC/AKT/AP‑1 signaling axis. Our data revealed a previously unknown tumor suppressor role of miR‑218 by blocking the TNC/AKT/AP‑1/TGFβ1‑positive feedback loop in glioma. Gliomas are the most malignant and common tumors of the human brain, and the prognosis of glioma patients is extremely poor. MicroRNAs (miRNAs or miRs) play critical roles in different types of cancer by performing post‑transcriptional regulation of gene expression. Although miR‑218 has been demonstrated to be decreased in gliomas, its role in gliomas remains largely unknown. miR‑218 expression was analyzed in gliomas and normal brain tissues (control subjects) using a dataset from The Cancer Genome Atlas. A series of and studies were performed to determine the biological roles of miR‑218 in glioma cells. Potential targets of miR‑218 were identified using a dual‑luciferase reporter system. Western blot and dual‑luciferase reporter system experiments were performed to evaluate the regulatory effect of miR‑218 on the tenascin C (TNC)/AKT/activator protein 1 (AP‑1)/transforming growth factor β1 (TGFβ1) pathway. It was demonstrated that miR‑218 was significantly downregulated in gliomas compared with control subjects, and played potent tumor suppressor roles in glioma cells by inhibiting cell proliferation, colony formation, migration, invasion and tumorigenic potential in nude mice, as well as inducing cell cycle arrest and apoptosis. Mechanistically, miR‑218 inhibited malignant phenotypes of glioma cells by binding to the 3'‑untranslated region of its target TNC and subsequently suppressing its expression. As a result, miR‑218 could reduce AKT phosphorylation and subsequently inhibit transcriptional activity of AP‑1 by reducing JNK phosphorylation, downregulating the expression of TGFβ1, while TGFβ1 was able to, in turn, activate the TNC/AKT/AP‑1 signaling axis. Our data revealed a previously unknown tumor suppressor role of miR‑218 by blocking the TNC/AKT/AP‑1/TGFβ1‑positive feedback loop in glioma. |
| ArticleNumber | 205 |
| Author | Hou, Peng Zhang, Rui Dang, Siwen Ji, Meiju Li, Gang Tian, Sijia |
| AuthorAffiliation | 2 Department of Neurosurgery, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi 710038, PR China 3 Center for Translational Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China 1 Key Laboratory for Tumor Precision Medicine of Shaanxi Province and Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China |
| AuthorAffiliation_xml | – name: 2 Department of Neurosurgery, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi 710038, PR China – name: 3 Center for Translational Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China – name: 1 Key Laboratory for Tumor Precision Medicine of Shaanxi Province and Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China |
| Author_xml | – sequence: 1 givenname: Siwen surname: Dang fullname: Dang, Siwen organization: Key Laboratory for Tumor Precision Medicine of Shaanxi Province and Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China – sequence: 2 givenname: Rui surname: Zhang fullname: Zhang, Rui organization: Key Laboratory for Tumor Precision Medicine of Shaanxi Province and Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China – sequence: 3 givenname: Sijia surname: Tian fullname: Tian, Sijia organization: Key Laboratory for Tumor Precision Medicine of Shaanxi Province and Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China – sequence: 4 givenname: Peng surname: Hou fullname: Hou, Peng organization: Key Laboratory for Tumor Precision Medicine of Shaanxi Province and Department of Endocrinology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China – sequence: 5 givenname: Gang surname: Li fullname: Li, Gang organization: Department of Neurosurgery, Tangdu Hospital, Air Force Medical University, Xi'an, Shaanxi 710038, PR China – sequence: 6 givenname: Meiju surname: Ji fullname: Ji, Meiju organization: Center for Translational Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, PR China |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/34558654$$D View this record in MEDLINE/PubMed |
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| Keywords | glioma AKT/activator protein 1/transforming growth factor β1 signaling axis tenascin C tumorigenesis microRNA‑218 |
| Language | English |
| License | https://creativecommons.org/licenses/by-nc-nd/4.0 This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
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publication-title: Oncogene doi: 10.1038/sj.onc.1207064 |
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| Snippet | Gliomas are the most malignant and common tumors of the human brain, and the prognosis of glioma patients is extremely poor MicroRNAs (miRNAs or miRs) play... Gliomas are the most malignant and common tumors of the human brain, and the prognosis of glioma patients is extremely poor. MicroRNAs (miRNAs or miRs) play... |
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| SubjectTerms | AKT/activator protein 1/transforming growth factor β1 signaling axis Animals Apoptosis - genetics Biotechnology Brain cancer Cancer therapies Cell cycle Cell Cycle Checkpoints - genetics Cell Proliferation - genetics Down-Regulation - genetics Experiments Feedback, Physiological Flow cytometry Gene expression Gene Expression Regulation, Neoplastic Glioma Glioma - genetics Glioma - pathology Laboratory animals Male Mice microRNA-218 MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism Phenotype Proto-Oncogene Proteins c-akt - metabolism Signal Transduction Survival analysis Tenascin - metabolism tenascin C Transcription Factor AP-1 - metabolism Transforming Growth Factor beta1 - metabolism Tumorigenesis Tumors |
| Title | MicroRNA-218 inhibits the malignant phenotypes of glioma by modulating the TNC/AKT/AP-1/TGFβ1 feedback signaling loop |
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