دورية أكاديمية

Mechanism of miR-143-3p inhibiting proliferation, migration and invasion of osteosarcoma cells by targeting MAPK7

التفاصيل البيبلوغرافية
العنوان: Mechanism of miR-143-3p inhibiting proliferation, migration and invasion of osteosarcoma cells by targeting MAPK7
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
الوصف
تدمد:21691401
2169141X
DOI:10.1080/21691401.2019.1620252