Up-Regulation of MiR-300 Promotes Proliferation and Invasion of Osteosarcoma by Targeting BRD7
Increasing reports suggest that deregulated microRNAs (miRNAs) might provide novel therapeutic targets for cancers. However, the expression and function of miR-300 in osteosarcoma is still unknown. In our study, we found that the expression of miR-300 was up-regulated in osteosarcoma tissues and cel...
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| Published in | PloS one Vol. 10; no. 5; p. e0127682 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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Public Library of Science
26.05.2015
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| Abstract | Increasing reports suggest that deregulated microRNAs (miRNAs) might provide novel therapeutic targets for cancers. However, the expression and function of miR-300 in osteosarcoma is still unknown. In our study, we found that the expression of miR-300 was up-regulated in osteosarcoma tissues and cells compared with paired adjacent non-tumor bone tissues and osteoblastic cells using RT-qPCR. The enforced expression of miR-300 could promote cell proliferation, invasion and epithelial-mesenchymal transition (EMT). Moreover, we identified that bromodomain-containing protein 7 (BRD7), a new tumor suppressor gene, was a direct target of miR-300. Ectopic expression of BRD7 could significantly inhibit miR-300-promoted proliferation, invasion and EMT. Therefore, our results identify an important role for miR-300 in osteosarcoma through regulating BRD7 expression. |
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| AbstractList | Increasing reports suggest that deregulated microRNAs (miRNAs) might provide novel therapeutic targets for cancers. However, the expression and function of miR-300 in osteosarcoma is still unknown. In our study, we found that the expression of miR-300 was up-regulated in osteosarcoma tissues and cells compared with paired adjacent non-tumor bone tissues and osteoblastic cells using RT-qPCR. The enforced expression of miR-300 could promote cell proliferation, invasion and epithelial-mesenchymal transition (EMT). Moreover, we identified that bromodomain-containing protein 7 (BRD7), a new tumor suppressor gene, was a direct target of miR-300. Ectopic expression of BRD7 could significantly inhibit miR-300-promoted proliferation, invasion and EMT. Therefore, our results identify an important role for miR-300 in osteosarcoma through regulating BRD7 expression. Increasing reports suggest that deregulated microRNAs (miRNAs) might provide novel therapeutic targets for cancers. However, the expression and function of miR-300 in osteosarcoma is still unknown. In our study, we found that the expression of miR-300 was up-regulated in osteosarcoma tissues and cells compared with paired adjacent non-tumor bone tissues and osteoblastic cells using RT-qPCR. The enforced expression of miR-300 could promote cell proliferation, invasion and epithelial-mesenchymal transition (EMT). Moreover, we identified that bromodomain-containing protein 7 (BRD7), a new tumor suppressor gene, was a direct target of miR-300. Ectopic expression of BRD7 could significantly inhibit miR-300-promoted proliferation, invasion and EMT. Therefore, our results identify an important role for miR-300 in osteosarcoma through regulating BRD7 expression.Increasing reports suggest that deregulated microRNAs (miRNAs) might provide novel therapeutic targets for cancers. However, the expression and function of miR-300 in osteosarcoma is still unknown. In our study, we found that the expression of miR-300 was up-regulated in osteosarcoma tissues and cells compared with paired adjacent non-tumor bone tissues and osteoblastic cells using RT-qPCR. The enforced expression of miR-300 could promote cell proliferation, invasion and epithelial-mesenchymal transition (EMT). Moreover, we identified that bromodomain-containing protein 7 (BRD7), a new tumor suppressor gene, was a direct target of miR-300. Ectopic expression of BRD7 could significantly inhibit miR-300-promoted proliferation, invasion and EMT. Therefore, our results identify an important role for miR-300 in osteosarcoma through regulating BRD7 expression. |
| Audience | Academic |
| Author | Zhao, Jindong Ni, Linying Xue, Zhen Niu, Liyuan Guo, Yashan An, Gang |
| AuthorAffiliation | Peking Union Medical College Hospital, CHINA 3 Department of Physical diagnosis, The Affiliated Hospital of Harbin Institute of Technology, Harbin, Heilongjiang Province, 150001, China 4 Department of Orthopaedic Surgery, The Tumor Hospital of Harbin Medical University, Harbin, Heilongjiang Province, 150086, China 2 Department of Orthopaedic Surgery, the Fifth Hospital of Harbin City, Harbin, Heilongjiang Province, 150040, China 1 Department of Orthopaedic Surgery, The Affiliated No.2 Hospital of Harbin Medical University, Harbin, Heilongjiang Province, 150086, China |
| AuthorAffiliation_xml | – name: 4 Department of Orthopaedic Surgery, The Tumor Hospital of Harbin Medical University, Harbin, Heilongjiang Province, 150086, China – name: 2 Department of Orthopaedic Surgery, the Fifth Hospital of Harbin City, Harbin, Heilongjiang Province, 150040, China – name: Peking Union Medical College Hospital, CHINA – name: 1 Department of Orthopaedic Surgery, The Affiliated No.2 Hospital of Harbin Medical University, Harbin, Heilongjiang Province, 150086, China – name: 3 Department of Physical diagnosis, The Affiliated Hospital of Harbin Institute of Technology, Harbin, Heilongjiang Province, 150001, China |
| Author_xml | – sequence: 1 givenname: Zhen surname: Xue fullname: Xue, Zhen – sequence: 2 givenname: Jindong surname: Zhao fullname: Zhao, Jindong – sequence: 3 givenname: Liyuan surname: Niu fullname: Niu, Liyuan – sequence: 4 givenname: Gang surname: An fullname: An, Gang – sequence: 5 givenname: Yashan surname: Guo fullname: Guo, Yashan – sequence: 6 givenname: Linying surname: Ni fullname: Ni, Linying |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26010572$$D View this record in MEDLINE/PubMed |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 ObjectType-Correction/Retraction-3 Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: ZX JZ LN GA YG LN. Performed the experiments: ZX JZ LN GA YG LN. Analyzed the data: ZX JZ LN GA YG LN. Contributed reagents/materials/analysis tools: ZX JZ LN GA YG LN. Wrote the paper: ZX JZ LN GA YG LN. |
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| SubjectTerms | Analysis of Variance Apoptosis Biocompatibility Blotting, Western Bone cancer Cell cycle Cell growth Cell Line, Tumor Cell proliferation Cell Proliferation - physiology Chromosomal Proteins, Non-Histone - metabolism Comparative analysis Deregulation Development and progression Ectopic expression Epithelial-Mesenchymal Transition - physiology Gene expression Gene Expression Regulation, Neoplastic - physiology Genetic aspects Health aspects Humans Luciferases Medical research Mesenchyme MicroRNA MicroRNAs MicroRNAs - metabolism miRNA Neoplasm Invasiveness - physiopathology Oligonucleotides - genetics Osteoblasts Osteosarcoma Osteosarcoma - physiopathology Physiological aspects Physiology Proteins Real-Time Polymerase Chain Reaction Sarcoma Surgery Tissues Tumor suppressor genes Variance analysis |
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| Title | Up-Regulation of MiR-300 Promotes Proliferation and Invasion of Osteosarcoma by Targeting BRD7 |
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