دورية أكاديمية

MicroRNA-29a-3p Downregulation Causes Gab1 Upregulation to Promote Glioma Cell Proliferation

التفاصيل البيبلوغرافية
العنوان: MicroRNA-29a-3p Downregulation Causes Gab1 Upregulation to Promote Glioma Cell Proliferation
المؤلفون: Nai-yuan Shao, Dong-xing Wang, Yin Wang, Ya Li, Zhi-qing Zhang, Qin Jiang, Weifeng Luo, Cong Cao
المصدر: Cellular Physiology and Biochemistry, Vol 48, Iss 2, Pp 450-460 (2018)
بيانات النشر: Cell Physiol Biochem Press GmbH & Co KG, 2018.
سنة النشر: 2018
المجموعة: LCC:Physiology
LCC:Biochemistry
مصطلحات موضوعية: Glioma, Gab1, MicroRNA-29a-3p, Cell proliferation, Physiology, QP1-981, Biochemistry, QD415-436
الوصف: Background/Aims: Glioma causes significant human mortalities annually. Molecularly-targeted therapy is a focus of glioma research. Methods: Grb2-associated binding 1 (Gab1) expression and microRNA-29a-3p (“miR-29a-3p”) expression in human glioma cells and tissues were tested by Western blotting assay and qRT-PCR assay. shRNA/siRNA strategy was applied to silence Gab1 in human glioma cells. miR-29a or anti-sense miR-29a construct was transfected to human glioma cells. Cell proliferation was tested by BrdU ELISA assay and cell counting assay. Results: We show that expression of Gab1 was significantly elevated in human glioma tissues and cells, which correlated with downregulation of its putative microRNA: miR-29a-3p. In A172 glioma cells and primary human glioma cells, Gab1 shRNA/siRNA inhibited Akt-Erk activation and cell proliferation. Forced-expression of miR-29a-3p downregulated Gab1, inhibiting glioma cell proliferation, whereas miR-29a-3p was in-effective on cell proliferation in Gab1-silenced A172 cells. Furthermore, introduction of a 3’-untranslated region (3’-UTR) mutant Gab1 (UTR-G160A) blocked miR-29a-3p-induced inhibition on Akt signaling and A172 cell proliferation. Conclusions: miR-29a-3p downregulation leads to Gab1 upregulation to promote glioma cell proliferation.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1015-8987
1421-9778
Relation: https://www.karger.com/Article/FullText/491776; https://doaj.org/toc/1015-8987; https://doaj.org/toc/1421-9778
DOI: 10.1159/000491776
URL الوصول: https://doaj.org/article/377dd2d759df450f99d71dea38f727d3
رقم الأكسشن: edsdoj.377dd2d759df450f99d71dea38f727d3
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:10158987
14219778
DOI:10.1159/000491776