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Sun, Gui-Li, Wang, Dong. (1399). Gallic acid from Terminalia chebula inhibited the growth of esophageal carcinoma cells by suppressing the Hippo signal pathway. , 23(11), 1401-1408. doi: 10.22038/ijbms.2020.42283.9982
Gui-Li Sun; Dong Wang. "Gallic acid from Terminalia chebula inhibited the growth of esophageal carcinoma cells by suppressing the Hippo signal pathway". , 23, 11, 1399, 1401-1408. doi: 10.22038/ijbms.2020.42283.9982
Sun, Gui-Li, Wang, Dong. (1399). 'Gallic acid from Terminalia chebula inhibited the growth of esophageal carcinoma cells by suppressing the Hippo signal pathway', , 23(11), pp. 1401-1408. doi: 10.22038/ijbms.2020.42283.9982
Sun, Gui-Li, Wang, Dong. Gallic acid from Terminalia chebula inhibited the growth of esophageal carcinoma cells by suppressing the Hippo signal pathway. , 1399; 23(11): 1401-1408. doi: 10.22038/ijbms.2020.42283.9982

Gallic acid from Terminalia chebula inhibited the growth of esophageal carcinoma cells by suppressing the Hippo signal pathway

Iranian Journal of Basic Medical Sciences
مقاله 6، دوره 23، شماره 11، بهمن 2020، صفحه 1401-1408    اصل مقاله (1.1 M)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22038/ijbms.2020.42283.9982
نویسندگان
Gui-Li Sun1؛ Dong Wang* 2
1Department of Oncology, Affiliated Hospital of Inner Mongolia University for Nationalities, Tongliao 028000, China
2Department Oncology of Mongolian-Western Medicine, Affiliated Hospital of Inner Mongolia University for Nationalities, Tongliao 028007, China
چکیده
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.
کلیدواژه‌ها
Apoptosis؛ Cell proliferation؛ Esophageal neoplasms؛ Gallic acid؛ Signal transduction
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