التفاصيل البيبلوغرافية
| العنوان: |
miRNA-1180 suppresses HCC cell activities via TRAF1/NF-κB signaling pathway |
| المؤلفون: |
ZHENG, Feng, WANG, Zheng |
| المصدر: |
Food Science and Technology. December 2020 40(2) |
| بيانات النشر: |
Sociedade Brasileira de Ciência e Tecnologia de Alimentos, 2020. |
| سنة النشر: |
2020 |
| مصطلحات موضوعية: |
miRNA-1180, HepG2, TRAF1, NF-κB, P53 |
| الوصف: |
The miRNA-1180 anti-cancer effects in hepatocellular carcinoma cell were studied. 33 hepatocellular carcinoma patients were collected. In cancer and adjacent normal tissue from patients, TRAF1 protein and miR-1180 expression was determined by HE staining, IHC and RT-PCR methods. In the cell experiments, HepG2 cells were divided into three groups: NC group, BL group and miRNA group. The cells of NC group were un-treated; BL group were transfected with empty camer; miRNA group were transfixed with miRNA-1180. We determinates cell proliferation rate of difference groups, measuring the cell apoptosis rate and cell cycle of difference groups by flow cytometry, detected cell invasion and migration abilities of difference groups by transwell and wound healing assay and evaluating relative proteins expressions by WB assay. Compared with Normal liver tissue, cell infiltrations were significantly increased. miR-1180 was negative correlation with TRAF. The cell proliferation rate of miRNA group was significantly lower than that of NC group; The cell apoptosis and G1 phase rates were significantly difference among three groups; however, P53 and P21 protein expressions were significantly increased in miRNA groups. Over-expression miRNA-1180 had effect to inhibit HepG2 cell proliferation, invasion, migration and improve HepG2 cell apoptosis by regulation TRAF1/NF-κB signaling pathway. |
| نوع الوثيقة: |
article |
| وصف الملف: |
text/html |
| اللغة: |
English |
| تدمد: |
0101-2061 |
| DOI: |
10.1590/fst.26219 |
| URL الوصول: |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0101-20612020000600626 |
| Rights: |
info:eu-repo/semantics/openAccess |
| رقم الانضمام: |
edssci.S0101.20612020000600626 |
| قاعدة البيانات: |
SciELO |