Quhui Wang1, Gang Wang2, Xiaodong Xu3, Zhong Chen4. 1. Department of General Surgery, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215000, China. 2. Department of Anesthesiology, Union Hospital Affiliated With Tongji Medical College of Huazhong University of Science and Technology, Wuhan, 430000, China. 3. Department of General Surgery, The 4th Affiliated Hospital of Nantong University, Yancheng, 224000, China. 4. Department of General Surgery, First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215000, China; Department of General Surgery, Affiliated Hospital of Nantong University, Nantong 226001, China. Electronic address: chenzgs@163.com.
Abstract
BACKGROUND: The purpose of our study was to investigate the roles of miR-760 and its potential mechanisms in HCC. METHODS: The functions of miR-760 were identified and measured by MTT, colony formation, transwell, and flow cytometry assays. Luciferase assay was applied to verify the direct binding of miR-760 on HMGA2 3'untranslated region (3'UTR). Then, in vitro experiment was used to investigate the biological effects of miR-760 and HMGA2. Luciferase and ChIP assays were used to detect the validity of SP1 binding sites on the miR-760 promoter. RESULTS: We demonstrated that miR-760 overexpression suppressed cell proliferation, migration, and invasion in HCC. Besides, HMGA2 was demonstrated as a direct target gene of miR-760. Furthermore, we found that methylation may result in the downregulation of miR-760, and SP1 could inhibit the transcription of miR-760. CONCLUSIONS: Our study demonstrated that SP1/miR-760/HMGA2 may serve as a molecular regulatory axis for HCC treatment.
BACKGROUND: The purpose of our study was to investigate the roles of miR-760 and its potential mechanisms in HCC. METHODS: The functions of miR-760 were identified and measured by MTT, colony formation, transwell, and flow cytometry assays. Luciferase assay was applied to verify the direct binding of miR-760 on HMGA2 3'untranslated region (3'UTR). Then, in vitro experiment was used to investigate the biological effects of miR-760 and HMGA2. Luciferase and ChIP assays were used to detect the validity of SP1 binding sites on the miR-760 promoter. RESULTS: We demonstrated that miR-760 overexpression suppressed cell proliferation, migration, and invasion in HCC. Besides, HMGA2 was demonstrated as a direct target gene of miR-760. Furthermore, we found that methylation may result in the downregulation of miR-760, and SP1 could inhibit the transcription of miR-760. CONCLUSIONS: Our study demonstrated that SP1/miR-760/HMGA2 may serve as a molecular regulatory axis for HCC treatment.