این سایت در حال حاضر پشتیبانی نمی شود و امکان دارد داده های نشریات بروز نباشند
صفحه اصلی
درباره پایگاه
فهرست سامانه ها
الزامات سامانه ها
فهرست سازمانی
تماس با ما
JCR 2016
جستجوی مقالات
سه شنبه 18 آذر 1404
Iranian Journal of Basic Medical Sciences
، جلد ۲۳، شماره ۱۱، صفحات ۱۴۰۱-۱۴۰۸
عنوان فارسی
چکیده فارسی مقاله
کلیدواژههای فارسی مقاله
عنوان انگلیسی
Gallic acid from Terminalia chebula inhibited the growth of esophageal carcinoma cells by suppressing the Hippo signal pathway
چکیده انگلیسی مقاله
Objective(s): To explore the molecular mechanism of gallic acid (GA) from Terminalia chebula in suppressing the growth of esophageal carcinoma (EC).Materials and Methods: Human EC cells (EC9706 and KYSE450) were treated with different concentrations of GA (10, 20, and 40 μg/ml), which were subjected to 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide (MTT) assay, plate clone formation assay, annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) staining, and Western blotting. EC mice were divided into model, 0.3% GA, and 1% GA groups to observe the tumor volume and the expressions of YAP, TAZ, Ki-67, and caspase-3 in tumor tissues. Results: GA decreased cell viability and colony formation of EC9706 and KYSE450 cells, which was more obvious as the concentration increased. In addition, GA promoted cell apoptosis in a concentration-dependent manner with the up-regulation of pro-apoptotic proteins (Bax, cleaved caspase-3, and cleaved caspase-9) and nuclear YAP/TAZ, as well as the down-regulation of anti-apoptotic protein Bcl-2 and the levels of p-YAP and p-TAZ. Moreover, GA decreased the growth of xenograft tumor in vivo, with the reduction in the tumor volume and the reduction of YAP and TAZ expressions in the tumor tissues. In addition, Ki-67 expression in GA groups was lower than those in the Model group, with the increase in caspase-3 expression in the tumor tissues. Changes aforementioned were obviously shown in the 0.3% GA group. Conclusion: GA blocked the activity of the Hippo pathway to suppress cell proliferation of EC and facilitate cell apoptosis, which is expected to be a novel strategy for treatment of EC.
کلیدواژههای انگلیسی مقاله
Apoptosis, Cell Proliferation, Esophageal neoplasms, Gallic acid, Signal transduction
نویسندگان مقاله
| Gui-Li Sun
Department of Oncology, Affiliated Hospital of Inner Mongolia University for Nationalities, Tongliao 028000, China
| Dong Wang
Department Oncology of Mongolian-Western Medicine, Affiliated Hospital of Inner Mongolia University for Nationalities, Tongliao 028007, China
نشانی اینترنتی
https://ijbms.mums.ac.ir/article_16433.html
فایل مقاله
فایلی برای مقاله ذخیره نشده است
کد مقاله (doi)
زبان مقاله منتشر شده
en
موضوعات مقاله منتشر شده
نوع مقاله منتشر شده
Original Article
برگشت به:
صفحه اول پایگاه
|
نسخه مرتبط
|
نشریه مرتبط
|
فهرست نشریات