Circ_0000069 contributes to the growth,metastasis and glutamine metabolism in renal cell carcinoma (RCC) via regulating miR-125a-5p-dependent SLC1A5 expression |
| |
| Institution: | 1. Department of Neurology, Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai City, Shandong Province, China;2. Department of Urology, Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai City, Shandong Province, China;1. Hematology, Graduate School of Medicine, Osaka City University, Osaka, Japan;2. Department of Diagnostic Pathology, Graduate School of Medicine, Osaka City University, Osaka, Japan;3. Department of Gastroenterology, Graduate School of Medicine, Osaka City University, Osaka, Japan;1. Department of Hematology, Children''s Hospital of Soochow University, Suzhou, China;2. Children''s Hematology and Oncology Center of Jiangsu Province, Jiangsu, China;1. Department of Transfusion Medicine, Histocompatibility and Molecular Biology, Jaypee Hospital, Noida, UP 201301, India;2. Department of Histocompatibility and Molecular Biology, Jaypee Hospital, Noida,UP 201301, India;3. Department of Transfusion Medicine, Jaypee Hospital, Noida, UP 201301, India;4. Kidney Transplant Programme, Department of Urology and Kidney Transplant, Jaypee Hospital, Noida, UP 201301, India;5. Department of Nephrology and Kidney Transplant, Jaypee Hospital, Noida, UP 201301, India;1. Department of Gastroenterology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, Zhejiang Province, China;2. Department of Gastroenterology, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo 315000, Zhejiang Province, China;3. Ningbo Institute of Life and Health Industry, University of Chinese Academy of Sciences, Ningbo 315000, Zhejiang Province, China;4. Department of Pharmacy, Hwa Mei Hospital, University of Chinese Academy of Sciences, Ningbo 315000, Zhejiang Province, China.;1. Department of Neurology, Guangzhou First People''s Hospital, School of Medicine, South China University of Technology, Guangzhou 510180, China;2. Department of Neurology, Guangzhou First People''s Hospital, Guangzhou Medical University, Guangzhou 510180, China;3. Department of Neurology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510180, China |
| |
| Abstract: | BackgroundCircular RNAs (circRNAs) have emerged as critical mediators in various cancers, including renal cell carcinoma (RCC). In the present research, the functions of circ_0000069 in RCC were explored.MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) assay, western blot assay and immunohistochemistry (IHC) assay were performed for the expression of circ_0000069, microRNA-125a-5p (miR-125a-5p) and solute carrier family 1 member 5 (SLC1A5). Cell Counting Kit-8 (CCK-8) assay and 5′-ethynyl-2′-deoxyuridine (EdU) assay were performed for cell proliferation. Flow cytometry assay was manipulated for cell apoptosis. Transwell assay and wound-healing assay were utilized for cell invasion and migration. Glutamine metabolism level was evaluated by examining glutamine consumption, α-ketoglutarate production and glutamate production. Dual-luciferase reporter assay was used to analyze the relationships of circ_0000069, miR-125a-5p and SLC1A5. Murine xenograft model assay was conducted to analyze the function of circ_0000069 in vivo.ResultsCirc_0000069 level was abnormally upregulated in RCC tissues and cells. Knockdown of circ_0000069 inhibited the proliferation, invasion, migration and glutamine metabolism and promoted the apoptosis in RCC cells in vitro and restrained tumor growth in vivo. Circ_0000069 served as the sponge for miR-125a-5p. MiR-125a-5p inhibition ameliorated the effects of circ_0000069 knockdown on RCC cell malignant behaviors. SLC1A5 was identified as the target gene of miR-125a-5p. Moreover, miR-125a-5p overexpression repressed the progression of RCC cells, while SLC1A5 elevation abrogated the effect.ConclusionCirc_0000069 knockdown inhibited the carcinogenesis of RCC by regulating miR-125a-5p/SLC1A5 axis. |
| |
| Keywords: | |
| 本文献已被 ScienceDirect 等数据库收录！ |
|
