MiR-367 negatively regulates apoptosis induced by adriamycin in osteosarcoma cells by targeting KLF4
Diverse functions of microRNAs have been investigated in tumorigenesis in osteosarcoma (OS), involving the regulation of proliferation, invasion, migration, apoptosis and drug resistance. MiR-367 was found to be an oncogene and increased in OS. However, the function of miR-367 in drug resistance in...
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pubmed-49081872016-06-22 MiR-367 negatively regulates apoptosis induced by adriamycin in osteosarcoma cells by targeting KLF4 Wang, Guang-Chao He, Qian-Yun Tong, Da-Ke Wang, Chuan-Feng Liu, Kang Ding, Chen Ji, Fang Zhang, Hao Research Paper Diverse functions of microRNAs have been investigated in tumorigenesis in osteosarcoma (OS), involving the regulation of proliferation, invasion, migration, apoptosis and drug resistance. MiR-367 was found to be an oncogene and increased in OS. However, the function of miR-367 in drug resistance in OS cells is still unknown. In this study, we found that miR-367 was up-regulated in OS tissues and OS cell cultures. Meanwhile, treatment with adriamycin (ADR) induced apoptosis of OS cells with upregulation of miR-367. Notably, KLF4 was demonstrated to be a direct target of miR-367 by gene reporter assay, and miR-367 significantly blocked both mRNA and protein level of KLF4. In addition, overexpression of miR-367 markedly suppressed the increase of KLF4 induced by ADR in OS cells, as well as Bax and cleaved caspase-3, which were significantly reversed by anti-miR-367 transfection. Taken together, our data demonstrates that miR-367 and KLF4 play important roles in OS treatment and ADR resistance, suggesting that miR-367 is a potential biomarker of chemotherapy resistance in OS and also probably a novel therapeutic target against OS. Elsevier 2016-02-17 /pmc/articles/PMC4908187/ /pubmed/27335771 http://dx.doi.org/10.1016/j.jbo.2016.02.002 Text en © 2016 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
repository_type |
Open Access Journal |
institution_category |
Foreign Institution |
institution |
US National Center for Biotechnology Information |
building |
NCBI PubMed |
collection |
Online Access |
language |
English |
format |
Online |
author |
Wang, Guang-Chao He, Qian-Yun Tong, Da-Ke Wang, Chuan-Feng Liu, Kang Ding, Chen Ji, Fang Zhang, Hao |
spellingShingle |
Wang, Guang-Chao He, Qian-Yun Tong, Da-Ke Wang, Chuan-Feng Liu, Kang Ding, Chen Ji, Fang Zhang, Hao MiR-367 negatively regulates apoptosis induced by adriamycin in osteosarcoma cells by targeting KLF4 |
author_facet |
Wang, Guang-Chao He, Qian-Yun Tong, Da-Ke Wang, Chuan-Feng Liu, Kang Ding, Chen Ji, Fang Zhang, Hao |
author_sort |
Wang, Guang-Chao |
title |
MiR-367 negatively regulates apoptosis induced by adriamycin in osteosarcoma cells by targeting KLF4 |
title_short |
MiR-367 negatively regulates apoptosis induced by adriamycin in osteosarcoma cells by targeting KLF4 |
title_full |
MiR-367 negatively regulates apoptosis induced by adriamycin in osteosarcoma cells by targeting KLF4 |
title_fullStr |
MiR-367 negatively regulates apoptosis induced by adriamycin in osteosarcoma cells by targeting KLF4 |
title_full_unstemmed |
MiR-367 negatively regulates apoptosis induced by adriamycin in osteosarcoma cells by targeting KLF4 |
title_sort |
mir-367 negatively regulates apoptosis induced by adriamycin in osteosarcoma cells by targeting klf4 |
description |
Diverse functions of microRNAs have been investigated in tumorigenesis in osteosarcoma (OS), involving the regulation of proliferation, invasion, migration, apoptosis and drug resistance. MiR-367 was found to be an oncogene and increased in OS. However, the function of miR-367 in drug resistance in OS cells is still unknown. In this study, we found that miR-367 was up-regulated in OS tissues and OS cell cultures. Meanwhile, treatment with adriamycin (ADR) induced apoptosis of OS cells with upregulation of miR-367. Notably, KLF4 was demonstrated to be a direct target of miR-367 by gene reporter assay, and miR-367 significantly blocked both mRNA and protein level of KLF4. In addition, overexpression of miR-367 markedly suppressed the increase of KLF4 induced by ADR in OS cells, as well as Bax and cleaved caspase-3, which were significantly reversed by anti-miR-367 transfection. Taken together, our data demonstrates that miR-367 and KLF4 play important roles in OS treatment and ADR resistance, suggesting that miR-367 is a potential biomarker of chemotherapy resistance in OS and also probably a novel therapeutic target against OS. |
publisher |
Elsevier |
publishDate |
2016 |
url |
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4908187/ |
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1613594766221508608 |