HOTAIR Promotes Cisplatin Resistance of Osteosarcoma Cells by Regulating Cell Proliferation, Invasion, and Apoptosis via miR-106a-5p/STAT3 Axis

被引:35
|
作者
Guo, Jiankuo [1 ]
Dou, Dongmei [2 ]
Zhang, Tianlun [3 ]
Wang, Bo [4 ]
机构
[1] Henan Univ, Dept Orthoped, Huaihe Hosp, Kaifeng, Henan, Peoples R China
[2] Henan Univ, Inst Slow Dis Risk Assessment, Kaifeng, Henan, Peoples R China
[3] Univ Elect Sci & Technol China, Sch Informat & Commun Engn, Chengdu, Sichuan, Peoples R China
[4] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Dept Orthoped, 1095 Jiefang St, Wuhan 430030, Hubei, Peoples R China
关键词
LncRNA HOTAIR; miR-106a-5p; STAT3; axis; cisplatin resistance; osteosarcoma; SIGNALING PATHWAY; DRUG-RESISTANCE; SUPPRESSES; MIGRATION; STAT3; CHEMORESISTANCE; OVEREXPRESSION; GROWTH;
D O I
10.1177/0963689720948447
中图分类号
Q813 [细胞工程];
学科分类号
摘要
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.
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页数:12
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