期刊
ONCOTARGET
卷 7, 期 46, 页码 75185-75196出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.12092
关键词
miR-424-5p; Smad3; proliferation; gastric cancer; TGF-beta signaling pathway
资金
- National Natural Science Foundation of China [81272712, 81572362]
- National Natural Science Foundation Project of International Cooperation(NSFC-NIH) [812111519]
- Priority Academic Program Development of Jiangsu Higher Education Institutions (PAPD) [JX10231801]
- Program for Development of Innovative Research Team in the First Affiliated Hospital of NJMU
- 333 Project of Jiangsu Province [BRA2015474]
MiRNAs have been reported to regulate gene expression and be associated with cancer progression. Recently, miR-424-5p was reported to play important role in a variety of tumors. However, the role and molecular mechanisms of miR-424-5p in GC (gastric cancer) remains largely unknown. In this study, we aimed to explore the role of miR-424-5p in GC. QRT-PCR was used to determine the expression levels of miR-424- 5p and Smad3. CCK8 assay, plate clone assay and cell cycle assay were used to measure the effects of miR-424-5p on GC cell proliferation. Luciferase reporter assay and western blotting were used to prove that Smad3 was one of the direct targets of miR-424-5p. Tumorigenesis assay was used to investigate the role of miR-424-5p in tumor growth of GC cells in vivo. We found that miR-424-5p was up-regulated in GC tissues and cells. Over-expression of miR-424-5p could promote the proliferation of GC cells. In addition, luciferase reporter assay and western blotting assay revealed that Smad3 was a direct target of miR-424-5p. Over-expression of Smad3 could partially reverse the effects of miR-424-5p on GC cell proliferation. Our study further revealed that miR-424-5p could inhibit TGF-beta signaling pathway by Smad3.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据