Abstract
Many microRNAs reside in clusters in the genome, are generally similar in sequence, are transcribed in the same direction, and usually function synergistically. The miR-183/96/182 cluster is composed of 3 miRNA genes, and increased expression of miR-183, 96 and 182 are implicated in glioma carcinogenesis. Knockdown of individual components or of the entire miR-183/96/182 cluster inhibits the survival of glioma cells by regulating the ROS-induced apoptosis pathway. Furthermore, inhibition of the miR-183/96/182 cluster induced ROS-mediated AKT/survival independent of three target genes FGF9, CPEB1, and FOXO1, and inhibition of the miRNA cluster induced p53/apoptosis signaling, which was dependent on these same genes. In addition, knockdown of the miR-183/96/182 cluster enhanced the anticancer effect of Temozolomide on glioma cells by the ROS-mediated apoptosis pathway. Therefore, the miR- 183/96/182 cluster may be a pleiotropic target for glioma therapy.
Keywords: AKT, apoptosis, glioma, micoRNA, miR-96, miR-182, miR-183, mitochondrial membrane potential, P53, temozolomide.
Current Cancer Drug Targets
Title:The miR-183/96/182 Cluster Regulates Oxidative Apoptosis and Sensitizes Cells to Chemotherapy in Gliomas
Volume: 13 Issue: 2
Author(s): Hailin Tang, Yanhui Bian, Chaofeng Tu, Zeyou Wang, Zhibin Yu, Qing Liu, Gang Xu, Minghua Wu and Guiyuan Li
Affiliation:
Keywords: AKT, apoptosis, glioma, micoRNA, miR-96, miR-182, miR-183, mitochondrial membrane potential, P53, temozolomide.
Abstract: Many microRNAs reside in clusters in the genome, are generally similar in sequence, are transcribed in the same direction, and usually function synergistically. The miR-183/96/182 cluster is composed of 3 miRNA genes, and increased expression of miR-183, 96 and 182 are implicated in glioma carcinogenesis. Knockdown of individual components or of the entire miR-183/96/182 cluster inhibits the survival of glioma cells by regulating the ROS-induced apoptosis pathway. Furthermore, inhibition of the miR-183/96/182 cluster induced ROS-mediated AKT/survival independent of three target genes FGF9, CPEB1, and FOXO1, and inhibition of the miRNA cluster induced p53/apoptosis signaling, which was dependent on these same genes. In addition, knockdown of the miR-183/96/182 cluster enhanced the anticancer effect of Temozolomide on glioma cells by the ROS-mediated apoptosis pathway. Therefore, the miR- 183/96/182 cluster may be a pleiotropic target for glioma therapy.
Export Options
About this article
Cite this article as:
Tang Hailin, Bian Yanhui, Tu Chaofeng, Wang Zeyou, Yu Zhibin, Liu Qing, Xu Gang, Wu Minghua and Li Guiyuan, The miR-183/96/182 Cluster Regulates Oxidative Apoptosis and Sensitizes Cells to Chemotherapy in Gliomas, Current Cancer Drug Targets 2013; 13 (2) . https://dx.doi.org/10.2174/1568009611313020010
DOI https://dx.doi.org/10.2174/1568009611313020010 |
Print ISSN 1568-0096 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5576 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
Related Articles
-
Inhibition of Apoptosis in Pediatric Cancer by Survivin
Current Pediatric Reviews Glycobiology in Malignant Gliomas: Expression and Functions of Galectins and Possible Therapeutic Options
Current Pharmaceutical Biotechnology Development of Curcumin-Loaded Solid Lipid Nanoparticles Utilizing Glyceryl Monostearate as Single Lipid Using QbD Approach: Characterization and Evaluation of Anticancer Activity Against Human Breast Cancer Cell Line
Current Drug Delivery Pregnancy, Programming and Preeclampsia: Gap Junctions at the Nexus of Pregnancy-induced Adaptation of Endothelial Function and Endothelial Adaptive Failure in PE
Current Vascular Pharmacology Nose-to-Brain Drug Delivery by Nanoparticles in the Treatment of Neurological Disorders
Current Medicinal Chemistry Leptomeningeal Metastasis: Challenges in Diagnosis and Treatment
Current Cancer Therapy Reviews Perspectives for Novel Mixed Diruthenium-Organic Drugs as Metallopharmaceuticals in Cancer Therapy
Anti-Cancer Agents in Medicinal Chemistry Inhibitor at the Gates, Inhibitor in the Chamber: Allosteric and Competitive Inhibitors of the Proteasome as Prospective Drugs
Current Medicinal Chemistry - Immunology, Endocrine & Metabolic Agents MicroRNA Polymorphisms, MicroRNA Pharmacogenomics and Cancer Susceptibility
Current Pharmacogenomics and Personalized Medicine Adhesion Mechanisms of the Lyme Disease Spirochete, Borrelia burgdorferi
Current Drug Targets - Infectious Disorders New Approaches With Natural Product Drugs for Overcoming Multidrug Resistance in Cancer
Current Pharmaceutical Design The Role of miR-129-5p in Cancer: A Novel Therapeutic Target
Current Molecular Pharmacology Peroxisome Proliferator Activated Receptor-Gamma Ligands as Potent Antineoplastic Agents
Current Medicinal Chemistry - Anti-Cancer Agents Glioma: Tryptophan Catabolite and Melatoninergic Pathways Link microRNA, 14-3- 3, Chromosome 4q35, Epigenetic Processes and other Glioma Biochemical Changes
Current Pharmaceutical Design Survivin Modulators: An Updated Patent Review (2011 - 2015)
Recent Patents on Anti-Cancer Drug Discovery Targeting the Voltage-Dependent K+ Channels Kv1.3 and Kv1.5 as Tumor Biomarkers for Cancer Detection and Prevention
Current Medicinal Chemistry bHLH Transcription Factors Inhibitors for Cancer Therapy: General Features for In Silico Drug Design
Current Medicinal Chemistry Anti-Tumor Effects of Osthole on Different Malignant Tissues: A Review of Molecular Mechanisms
Anti-Cancer Agents in Medicinal Chemistry Role of Hydrogen Sulfide and Polysulfides in Neurological Diseases: Focus on Protein S-Persulfidation
Current Neuropharmacology 5-HT5 Receptors
Current Drug Targets - CNS & Neurological Disorders