Long Non-Coding RNA Taurine Upregulated Gene 1 Targets miR-185 to Regulate Cell Proliferation and Glycolysis in Acute Myeloid Leukemia Cells in vitro
| Autor: | Jing Zhang, Weide Zhang, Ni Zheng, Yuhua Liu |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Gene knockdown Chemistry Cell growth Myeloid leukemia Transfection glycolysis TUG1 OncoTargets and Therapy miR-185 03 medical and health sciences Haematopoiesis 030104 developmental biology 0302 clinical medicine Oncology Downregulation and upregulation AML 030220 oncology & carcinogenesis Cancer research Pharmacology (medical) MTT assay Viability assay Original Research |
| Zdroj: | OncoTargets and therapy |
| ISSN: | 1178-6930 |
| Popis: | Weide Zhang,1,* Yuhua Liu,2,* Jing Zhang,3 Ni Zheng4 1Department of Hematology, The People’s Hospital of Shouguang, Shouguang, Shandong, People’s Republic of China; 2Department of Digestive Oncology, The Gansu Provincial Cancer Hospital, Lanzhou, Gansu, People’s Republic of China; 3Department of Psychiatry, Shouguang Mental and Health Care Center, Shouguang, Shandong, People’s Republic of China; 4Department of Clinical Laboratory, Shengli Oilfield Central Hospital, Dongying, Shandong, People’s Republic of China*These authors contributed equally to this workCorrespondence: Ni ZhengDepartment of Clinical Laboratory, Shengli Oilfield Central Hospital, No. 31 Jinan Road, Dongying 257034, Shandong, People’s Republic of ChinaTel +86-5468770171Email yb4445050youyaf@163.comBackground: Acute myeloid leukemia (AML) is a group of malignant hematopoietic system diseases. Taurine-upregulated gene 1 (TUG1) is a long non-coding RNA that has been associated with human cancers, including AML. However, the role and molecular mechanisms of TUG1 in AML remains to be defined.Methods: Expression of TUG1 and miR-185 was detected using RT-qPCR. Cell viability and apoptotic rate were measured by MTT assay and flow cytometry, respectively. Glycolysis was determined by commercial glucose and lactate assay kits and Western blot. The target binding between TUG1 and miR-185 was predicted on Starbase online database and confirmed by luciferase reporter assay and RNA immunoprecipitation.Results: TUG1 was upregulated and miR-185 was downregulated in the peripheral blood mononuclear cells of AML specimens and cells (HL-60, KG-1, MOLM-14, and MOLM-13). Both TUG1 knockdown and miR-185 overexpression via transfection could suppress cell viability, glucose consumption, lactate production, and hexokinase 2 expression, but promote apoptotic rate in HL-60 and KG-1 cells. Notably, TUG1 functioned as a sponge of miR-185 by target binding. Moreover, downregulation of miR-185 could partially overturn the effect of TUG1 knockdown on cell proliferation and glycolysis in HL-60 and KG-1 cells.Conclusion: Expression of TUG1 was upregulated in AML patients and cells, and its knockdown repressed cell proliferation and glycolysis in AML cells in vitro by targeting miR-185.Keywords: TUG1, miR-185, glycolysis, AML |
| Databáze: | OpenAIRE |
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