کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5558214 | 1561126 | 2017 | 7 صفحه PDF | دانلود رایگان |
- AMI-1 showed antitumor effects on gastric cancer (GC) cells in vitro and in vivo.
- AMI-1 downregulated PRMT5 and eIF4E expression and induced apoptosis in GC cells.
- AMI-1 targeted PRMT5 to inhibit GC cell proliferation.
Arginine methylation is carried out by protein arginine methyltransferase (PRMTs) family. Arginine methyltransferase inhibitor 1 (AMI-1) is mainly used to inhibit type I PRMT activity in vitro. However, the effects of AMI-1 on type II PRMT5 activity and gastric cancer (GC) remain unclear. In this study, we provided the first evidence that AMI-1 significantly inhibited GC cell proliferation and migration while induced GC cell apoptosis, and reduced the expression of PRMT5, eukaryotic translation initiation factor 4E (eIF4E), symmetric dimethylation of histone 3 (H3R8me2s) and histone 4 (H4R3me2s). In addition, AMI-1 inhibited tumor growth, downregulated eIF4E, H4R3me2s and H3R8me2s expression in mice xenografts model of GC. Collectively, our results suggest that AMI-1 inhibits GC by downregulating eIF4E and targeting type II PRMT5.
Journal: Toxicology and Applied Pharmacology - Volume 336, 1 December 2017, Pages 1-7