دورية أكاديمية
Mechanism of miR-143-3p inhibiting proliferation, migration and invasion of osteosarcoma cells by targeting MAPK7
العنوان: | Mechanism of miR-143-3p inhibiting proliferation, migration and invasion of osteosarcoma cells by targeting MAPK7 |
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المؤلفون: | Yu Hou, Helin Feng, Jianbao Jiao, Ligang Qian, Bo Sun, Pingtao Chen, Qinggui Li, Zhixing Liang |
المصدر: | Artificial Cells, Nanomedicine, and Biotechnology, Vol 47, Iss 1, Pp 2065-2071 (2019) |
بيانات النشر: | Taylor & Francis Group, 2019. |
سنة النشر: | 2019 |
المجموعة: | LCC:Biotechnology LCC:Medical technology |
مصطلحات موضوعية: | MiR-143-3p, mitogen-activated protein kinase 7, OS, migration, invasion, Biotechnology, TP248.13-248.65, Medical technology, R855-855.5 |
الوصف: | Objective To investigate the effects of miR-143-3p and MAPK7 on the proliferation, migration, and invasion of U2OS human osteosarcoma (OS) cells.Methods The expression of miR-143-3p and MAPK7 in U2OS cells were detected by qRT-PCR, and the protein level of MAPK7 was measured by western blot assay. The targeting relationship between miR-143-3p and MAPK7 was predicted by TargetScan and verified by dual luciferase reporter assay. MTT and Transwell assays were used to detect cell viability, migrated cells and invaded cells of U2OS cells.Results Compared with hFOB1.19 cells, the expression of miR-143-3p was down-regulated and MAPK7 was up-regulated in U2OS cells. Cell viability, migration and invasion ability significantly decreased induced by miR-143-3p overexpression or MAPK7 knockdown in U2OS cells. The results of dual luciferase reporter assay indicated that miR-143-3p interacted with MAPK7. Furthermore, overexpression of MAPK7 could reverse the inhibitory effects on cell proliferation, migration and invasion in U2OS cells induced by miR-143-3p mimics.Conclusion miR-143-3p could inhibit proliferation, migration and invasion of U2OS cells by targeting MAPK7. |
نوع الوثيقة: | article |
وصف الملف: | electronic resource |
اللغة: | English |
تدمد: | 21691401 2169-141X 2169-1401 |
Relation: | https://doaj.org/toc/2169-1401; https://doaj.org/toc/2169-141X |
DOI: | 10.1080/21691401.2019.1620252 |
URL الوصول: | https://doaj.org/article/edca9afa1c194a7cb8e220cbe67e885e |
رقم الأكسشن: | edsdoj.9afa1c194a7cb8e220cbe67e885e |
قاعدة البيانات: | Directory of Open Access Journals |
تدمد: | 21691401 2169141X |
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DOI: | 10.1080/21691401.2019.1620252 |