دورية أكاديمية
MicroRNA-29a-3p Downregulation Causes Gab1 Upregulation to Promote Glioma Cell Proliferation
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 |
تدمد: | 10158987 14219778 |
---|---|
DOI: | 10.1159/000491776 |