|کد مقاله||کد نشریه||سال انتشار||مقاله انگلیسی||ترجمه فارسی||نسخه تمام متن|
|2136072||1401595||2016||6 صفحه PDF||سفارش دهید||دانلود رایگان|
• miR-367 functions as an oncogene in OS targeting the tumor suppressor KLF4.
• ADR induces apoptosis in OS via miR-367/KLF4/Bax signaling pathway.
• miR-367 enhances the resistance of ADR to OS cells through suppressing KLF4.
• miR-367 could be a potential biomarker of chemotherapy resistance against OS.
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.
Journal: Journal of Bone Oncology - Volume 5, Issue 2, June 2016, Pages 51–56