کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8721927 | 1589451 | 2018 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Effects of miR-340 on hepatocellular carcinoma by targeting the DcR3 gene
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موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
غدد درون ریز، دیابت و متابولیسم
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چکیده انگلیسی
In hepatocellular carcinoma (HCC), miR-340 plays a vital role in the regulation of tumor occurrence and deterioration, while DcR3 gene is involved in cancer cell proliferation and apoptosis. This study analyzed miR-340 in the serum of patients with HCC and healthy controls. Then, miR-340, DcR3, TGF-β1 and Smad2 expression were measured in HCC tissues and adjacent parts. Relationship between miR-340 and DcR3 was verified. Effects of miR-340 on human HepG2 cell proliferation and apoptosis were explored. miR-340, DcR3, TGF-β1, Smad2 mRNA and protein expression were also determined after miR-340 transfection. Compared with the control, miR-340 was significantly lower in the serum of the HCC patients (pâ¯<â¯0.01). miR-340 was lower in HCC tissues than in adjacent; however, DcR3, TGF-β1 and Smad2 were higher (pâ¯<â¯0.01). Furthermore, luciferase activity was significantly lower in the cells co-transfected with miR-340 mimics and DcR3-3â²UTR-WT (pâ¯<â¯0.01), indicating that DcR3 was a target gene of miR-340. Moreover, decreased expression in DcR3, TGF-β1 and Smad2 was detected after miR-340 overexpression (pâ¯<â¯0.01), thus promoting apoptosis and blocking the proliferation of human HepG2 cells (pâ¯<â¯0.05). Furthermore, overexpression of DcR3 could activate the TGF-β1/Smad2 signal transduction pathway and increase the phosphorylation of Smad2. In conclusion, miR-340 plays a suppressive role in HCC development by targeting DcR3 and silencing the TGF-β1/Smad2 signaling pathway.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Digestive and Liver Disease - Volume 50, Issue 3, March 2018, Pages 291-296
Journal: Digestive and Liver Disease - Volume 50, Issue 3, March 2018, Pages 291-296
نویسندگان
Lijuan Xie, Zhuo Chen, Hongyu Liu, Lianyue Guan, Zhanpeng Wang, Wei Li,