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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.
Affiliation
  • Wang GC; Department of Orthopedics, Changhai Hospital, The Second Military Medical University, 168 Changhai Road, Shanghai 200433, China.
  • He QY; Department of Orthopedics, Changhai Hospital, The Second Military Medical University, 168 Changhai Road, Shanghai 200433, China.
  • Tong DK; Department of Orthopedics, Changhai Hospital, The Second Military Medical University, 168 Changhai Road, Shanghai 200433, China.
  • Wang CF; Department of Orthopedics, Changhai Hospital, The Second Military Medical University, 168 Changhai Road, Shanghai 200433, China.
  • Liu K; Department of Orthopedics, Changhai Hospital, The Second Military Medical University, 168 Changhai Road, Shanghai 200433, China.
  • Ding C; Department of Orthopedics, Changhai Hospital, The Second Military Medical University, 168 Changhai Road, Shanghai 200433, China.
  • Ji F; Department of Orthopedics, Changhai Hospital, The Second Military Medical University, 168 Changhai Road, Shanghai 200433, China.
  • Zhang H; Department of Orthopedics, Changhai Hospital, The Second Military Medical University, 168 Changhai Road, Shanghai 200433, China.
J Bone Oncol ; 5(2): 51-6, 2016 Jun.
Article in En | MEDLINE | ID: mdl-27335771
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.
Key words

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: J Bone Oncol Year: 2016 Document type: Article Affiliation country: Country of publication:

Full text: 1 Collection: 01-internacional Database: MEDLINE Language: En Journal: J Bone Oncol Year: 2016 Document type: Article Affiliation country: Country of publication: