期刊
JOURNAL OF BONE ONCOLOGY
卷 5, 期 2, 页码 51-56出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.jbo.2016.02.002
关键词
MiR-367; Osteosarcoma; Adriamycin; KLF4; Apoptosis; Chemotherapy resistance
类别
资金
- National Natural Science Foundation of China [81272942, 30973019, 81202122]
- Shanghai Science Foundation [10411956000]
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. (C) 2016 The Authors. Published by Elsevier GmbH.
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