机构：[1]Department of Orthopedics, Huaihe Hospital of Henan University, Kaifeng, Henan Province, China[2]Institute for Slow Disease Risk Assessment, Henan University, Kaifeng, Henan Province, China[3]School of Information and Communication Engineering, University of Electronic Science and Technology of China, Chengdu, Sichuan Province, China[4]Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China华中科技大学同济医学院附属同济医院
Osteosarcoma (OS) is a common primary malignant bone tumor among adolescences, and the emergence of multidrug resistance poses a huge challenge for clinical treatment of OS. LncRNA HOTAIR (HOX antisense intergenic RNA) has been reported to be associated with many malignancies, including OS. However, the underlying mechanisms of HOTAIR involved in drug resistance in OS are obscure. Our study showed that HOTAIR was upregulated in cisplatin (DDP)-resistant OS tissues and cells. HOTAIR knockdown decreased the DDP resistance, drug resistance-related gene expression, cell proliferation, and invasion and promoted apoptosis of Saos2/DDP, MG-63/DDP, and U2OS/DDP cells. Mechanism researches displayed that miR-106a-5p was downregulated in DDP-resistant OS tissues and cells. MiR-106a-5p directly bound with HOTAIR and was regulated by HOTAIR. Moreover, STAT3 was inhibited by miR-106a-5p at a post-transcriptional level, and the transfection of miR-106a-5p reversed the upregulation of STAT3 caused by HOTAIR overexpression. The increase or decrease of miR-106a-5p suppressed the effect of HOTAIR upregulation or downregulation on DDP resistance, cell proliferation, invasion, and apoptosis of Saos2/DDP, MG-63/DDP, and U2OS/DDP cells. What's more, the transfection of STAT3 siRNA reversed the decrease of DDP resistance, cell proliferation, and invasion and rescued the increase of apoptosis induced by miR-106a-5p inhibition. These data suggested that HOTAIR enhanced DDP resistance of Saos2/DDP, MG-63/DDP, and U2OS/DDP cells by affecting cell proliferation, invasion, and apoptosis via miR-106a-5p/STAT3 axis.
语种：
外文
被引次数：
WOS：
PubmedID：
中科院(CAS)分区：
出版当年[2020]版：
大类|3 区医学
小类|3 区医学：研究与实验3 区移植4 区细胞与组织工程
最新[2023]版：
大类|4 区医学
小类|4 区细胞与组织工程4 区医学：研究与实验4 区移植
JCR分区：
出版当年[2020]版：
Q2TRANSPLANTATIONQ2MEDICINE, RESEARCH & EXPERIMENTALQ3CELL & TISSUE ENGINEERING
最新[2023]版：
Q2MEDICINE, RESEARCH & EXPERIMENTALQ2TRANSPLANTATIONQ3CELL & TISSUE ENGINEERING
第一作者机构：[1]Department of Orthopedics, Huaihe Hospital of Henan University, Kaifeng, Henan Province, China
共同第一作者：
通讯作者：
通讯机构：[4]Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei Province, China[*1]Department of Orthopedics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1095 Jiefang Street, Wuhan 430030, Hubei Province, China
推荐引用方式(GB/T 7714)：
Guo Jiankuo,Dou Dongmei,Zhang Tianlun,et al.HOTAIR Promotes Cisplatin Resistance of Osteosarcoma Cells by Regulating Cell Proliferation, Invasion, and Apoptosis via miR-106a-5p/STAT3 Axis.[J].CELL TRANSPLANTATION.2020,29:doi:10.1177/0963689720948447.
APA：
Guo Jiankuo,Dou Dongmei,Zhang Tianlun&Wang Bo.(2020).HOTAIR Promotes Cisplatin Resistance of Osteosarcoma Cells by Regulating Cell Proliferation, Invasion, and Apoptosis via miR-106a-5p/STAT3 Axis..CELL TRANSPLANTATION,29,
MLA：
Guo Jiankuo,et al."HOTAIR Promotes Cisplatin Resistance of Osteosarcoma Cells by Regulating Cell Proliferation, Invasion, and Apoptosis via miR-106a-5p/STAT3 Axis.".CELL TRANSPLANTATION 29.(2020)
