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miR-34 inhibits growth and promotes apoptosis of osteosarcoma in nude mice through targetly regulating TGIF2 expression
miR-34 was reported to be involved in multiple tumors occurrence and development. The aim of the present study was to explore the impact of miR-34 on osteosarcoma and related mechanisms. Tumor tissues and non-tumor tissues of 34 patients with osteosarcoma were collected. qRT-PCR detection revealed t...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5997800/ https://www.ncbi.nlm.nih.gov/pubmed/29895719 http://dx.doi.org/10.1042/BSR20180078 |
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author | Xi, Liang Zhang, Yongfeng Kong, Shengnan Liang, Wei |
author_facet | Xi, Liang Zhang, Yongfeng Kong, Shengnan Liang, Wei |
author_sort | Xi, Liang |
collection | PubMed |
description | miR-34 was reported to be involved in multiple tumors occurrence and development. The aim of the present study was to explore the impact of miR-34 on osteosarcoma and related mechanisms. Tumor tissues and non-tumor tissues of 34 patients with osteosarcoma were collected. qRT-PCR detection revealed that miR-34 was significantly down-regulated in tumor tissues (P<0.05). hFOB 1.19 and MG-63 cells were cultured. qRT-PCR detection showed that miR-34 was also significantly down-regulated in MG-63 cells (P<0.05). After transfection by miR-34 mimics, MG-63 cells proliferation in nude mice was significantly impaired (P<0.05), and percentage of apoptosis as well as caspase-3 positive cells proportion of osteosarcoma tissue in nude mice was markly increased (P<0.05). Western blot and immunofluorescence results also demonstrated that TGIF2 relative expression and TGIF2 positive cells proportion were both dramatically decreased (P<0.05). By luciferase reporter assay, we found that TGIF2 was the target gene of miR-34. After transfected by TGIF2 overexpression vector or co-transfected by miR-34 mimics and TGIF2 overexpression vector, we observed that, compared with blank group, tumor volume was significantly increased and apoptotic cells as well as caspase-3 positive cells proportion was obviously decreased in TGIF2 group (P<0.05), while no significant difference was found in these indicators between blank group and TGIF2 + mimics group. We concluded that miR-34 inhibited growth and promoted apoptosis of osteosarcoma in nude mice through targetting regulated TGIF2 expression. |
format | Online Article Text |
id | pubmed-5997800 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-59978002018-06-13 miR-34 inhibits growth and promotes apoptosis of osteosarcoma in nude mice through targetly regulating TGIF2 expression Xi, Liang Zhang, Yongfeng Kong, Shengnan Liang, Wei Biosci Rep Research Articles miR-34 was reported to be involved in multiple tumors occurrence and development. The aim of the present study was to explore the impact of miR-34 on osteosarcoma and related mechanisms. Tumor tissues and non-tumor tissues of 34 patients with osteosarcoma were collected. qRT-PCR detection revealed that miR-34 was significantly down-regulated in tumor tissues (P<0.05). hFOB 1.19 and MG-63 cells were cultured. qRT-PCR detection showed that miR-34 was also significantly down-regulated in MG-63 cells (P<0.05). After transfection by miR-34 mimics, MG-63 cells proliferation in nude mice was significantly impaired (P<0.05), and percentage of apoptosis as well as caspase-3 positive cells proportion of osteosarcoma tissue in nude mice was markly increased (P<0.05). Western blot and immunofluorescence results also demonstrated that TGIF2 relative expression and TGIF2 positive cells proportion were both dramatically decreased (P<0.05). By luciferase reporter assay, we found that TGIF2 was the target gene of miR-34. After transfected by TGIF2 overexpression vector or co-transfected by miR-34 mimics and TGIF2 overexpression vector, we observed that, compared with blank group, tumor volume was significantly increased and apoptotic cells as well as caspase-3 positive cells proportion was obviously decreased in TGIF2 group (P<0.05), while no significant difference was found in these indicators between blank group and TGIF2 + mimics group. We concluded that miR-34 inhibited growth and promoted apoptosis of osteosarcoma in nude mice through targetting regulated TGIF2 expression. Portland Press Ltd. 2018-06-12 /pmc/articles/PMC5997800/ /pubmed/29895719 http://dx.doi.org/10.1042/BSR20180078 Text en © 2018 The Author(s). http://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (http://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research Articles Xi, Liang Zhang, Yongfeng Kong, Shengnan Liang, Wei miR-34 inhibits growth and promotes apoptosis of osteosarcoma in nude mice through targetly regulating TGIF2 expression |
title | miR-34 inhibits growth and promotes apoptosis of osteosarcoma in nude mice through targetly regulating TGIF2 expression |
title_full | miR-34 inhibits growth and promotes apoptosis of osteosarcoma in nude mice through targetly regulating TGIF2 expression |
title_fullStr | miR-34 inhibits growth and promotes apoptosis of osteosarcoma in nude mice through targetly regulating TGIF2 expression |
title_full_unstemmed | miR-34 inhibits growth and promotes apoptosis of osteosarcoma in nude mice through targetly regulating TGIF2 expression |
title_short | miR-34 inhibits growth and promotes apoptosis of osteosarcoma in nude mice through targetly regulating TGIF2 expression |
title_sort | mir-34 inhibits growth and promotes apoptosis of osteosarcoma in nude mice through targetly regulating tgif2 expression |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5997800/ https://www.ncbi.nlm.nih.gov/pubmed/29895719 http://dx.doi.org/10.1042/BSR20180078 |
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