Xiaorui Wang1,2,3,4,5,6, Zhongsheng Tong1,2,3,4,5, Hong Liu2,3,4,5,6,7. 1. Department of Breast Oncology, Tianjin Medical University Cancer Institute and Hospital, Tianjin City 300060, People's Republic of China. 2. National Clinical Research Center for Cancer, Tianjin City 300060, People's Republic of China. 3. Key Laboratory of Breast Cancer Prevention and Therapy, Tianjin City 300060, People's Republic of China. 4. Tianjin's Clinical Research Center for Cancer, Tianjin City 300060, People's Republic of China. 5. Key Laboratory of Cancer Prevention and Therapy, Tianjin City 300060, People's Republic of China. 6. Tianjin Medical University, Ministry of Education, Tianjin City 300060, People's Republic of China. 7. The Second Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, Tianjin City 300060, People's Republic of China.
Abstract
PURPOSE: This research was to investigate the role of miR-223-3p targeting epithelial cell transforming sequence 2 oncogene (ECT2) in activity, apoptosis, invasion and migration of MDA-MB-468 breast cancer (BC) cells. METHODS: The human BC cell lines MDA-MB-468 were used for the experiment. They were divided into six groups: blank group (no plasmid transfection), NC group (negative control, transfected empty plasmid), miR-223-3p mimic group (transfected miR-223-3p mimic plasmid), miR-223-3p inhibitor group (transfected miR-223-3p inhibitor plasmid), si-ECT2 group (transfected si ECT2 plasmid) and miR-223-3p mimic+oe-ECT2 group (transfected with miR-223-3p mimic plasmid and ECT2 plasmid). RESULTS: Compared with the NC group, the mRNA and protein expression of Bax in miR-223-3p mimic and si-ECT2 groups were significantly increased, while the mRNA and protein expression of ECT2, Bcl-2, vascular endothelial growth factor (VEGF), and TGF-β1 were significantly decreased (all P<0.05). Compared with the NC group, the expression of miR-223-3p and the mRNA and protein expression of Bax were significantly decreased in the miR-223-3p inhibitor group, while the mRNA and protein expression of ECT2, Bcl-2, VEGF and TGF-β1 were significantly increased (both P<0.05). Compared with the single processing group, the mRNA and protein expression of Bax in the miR-223-3p mimic+si-ECT2 group were significantly increased, while the mRNA and protein expression of ECT2, Bcl-2, VEGF, and TGF-β1 were significantly decreased (all P<0.05). CONCLUSION: MiR-223-3p targets and inhibits the expression of ECT2, thus inhibiting the invasion and migration of BC cells, and promoting cell apoptosis. miR-223-3p plays a protective role in BC.
PURPOSE: This research was to investigate the role of miR-223-3p targeting epithelial cell transforming sequence 2 oncogene (ECT2) in activity, apoptosis, invasion and migration of MDA-MB-468 breast cancer (BC) cells. METHODS: The human BC cell lines MDA-MB-468 were used for the experiment. They were divided into six groups: blank group (no plasmid transfection), NC group (negative control, transfected empty plasmid), miR-223-3p mimic group (transfected miR-223-3p mimic plasmid), miR-223-3p inhibitor group (transfected miR-223-3p inhibitor plasmid), si-ECT2 group (transfected si ECT2 plasmid) and miR-223-3p mimic+oe-ECT2 group (transfected with miR-223-3p mimic plasmid and ECT2 plasmid). RESULTS: Compared with the NC group, the mRNA and protein expression of Bax in miR-223-3p mimic and si-ECT2 groups were significantly increased, while the mRNA and protein expression of ECT2, Bcl-2, vascular endothelial growth factor (VEGF), and TGF-β1 were significantly decreased (all P<0.05). Compared with the NC group, the expression of miR-223-3p and the mRNA and protein expression of Bax were significantly decreased in the miR-223-3p inhibitor group, while the mRNA and protein expression of ECT2, Bcl-2, VEGF and TGF-β1 were significantly increased (both P<0.05). Compared with the single processing group, the mRNA and protein expression of Bax in the miR-223-3p mimic+si-ECT2 group were significantly increased, while the mRNA and protein expression of ECT2, Bcl-2, VEGF, and TGF-β1 were significantly decreased (all P<0.05). CONCLUSION: MiR-223-3p targets and inhibits the expression of ECT2, thus inhibiting the invasion and migration of BC cells, and promoting cell apoptosis. miR-223-3p plays a protective role in BC.
Authors: Molly A Taylor; Khalid Sossey-Alaoui; Cheryl L Thompson; David Danielpour; William P Schiemann Journal: J Clin Invest Date: 2012-12-17 Impact factor: 14.808
Authors: Harold J Burstein; Anthony D Elias; Hope S Rugo; Melody A Cobleigh; Antonio C Wolff; Peter D Eisenberg; Mary Lehman; Bonne J Adams; Carlo L Bello; Samuel E DePrimo; Charles M Baum; Kathy D Miller Journal: J Clin Oncol Date: 2008-03-17 Impact factor: 44.544
Authors: Hanna Aula; Tanja Skyttä; Suvi Tuohinen; Tiina Luukkaala; Mari Hämäläinen; Vesa Virtanen; Pekka Raatikainen; Eeva Moilanen; Pirkko-Liisa Kellokumpu-Lehtinen Journal: Radiat Oncol Date: 2018-10-19 Impact factor: 3.481