دورية أكاديمية
Baicalein facilitates gastric cancer cell apoptosis by triggering endoplasmic reticulum stress via repression of the PI3K/AKT pathway
| العنوان: | Baicalein facilitates gastric cancer cell apoptosis by triggering endoplasmic reticulum stress via repression of the PI3K/AKT pathway |
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| المؤلفون: | Junjie Shen, Zhiwen Yang, Xinlin Wu, Guodong Yao, Mingxing Hou |
| المصدر: | Applied Biological Chemistry, Vol 66, Iss 1, Pp 1-14 (2023) |
| بيانات النشر: | SpringerOpen, 2023. |
| سنة النشر: | 2023 |
| المجموعة: | LCC:Agriculture (General) LCC:Chemistry |
| مصطلحات موضوعية: | Baicalein, Gastric cancer, PI3K/AKT, Endoplasmic reticulum stress, BTG3, Cell apoptosis, Agriculture (General), S1-972, Chemistry, QD1-999 |
| الوصف: | Abstract Objective Gastric cancer (GC) remains a prevailing threat to life. Baicalein exhibits anti-cancer properties. This study estimated the mechanism of baicalein in GC cell apoptosis by mediating endoplasmic reticulum stress (ERS) through the PI3K/AKT pathway. Methods After treatment with different concentrations of baicalein, GC cell (HGC-27 and AGS) viability was detected by MTT assay. AGS cells more sensitive to baicalein treatment were selected as study subjects. The IC50 of baicalein on AGS cells was determined. Colony formation, cell cycle, and apoptosis were detected using crystal violet staining and flow cytometry. Levels of ERS-related and BTG3/PI3K/AKT pathway-related proteins were determined by Western blot. Intracellular Ca2+ level was measured using Fluo-3 AM fluorescence working solution. GC mouse models were established by subcutaneously injecting AGS cells into the right rib and were intragastrically administrated with baicalein. Tumor volume and weight were recorded. Expression of Ki67 in tumor tissues and positive expression of apoptotic cells were detected by immunohistochemistry and TUNEL staining. Results Baicalein inhibited cell proliferation and induced G0/G1 arrest and apoptosis by regulating the cell cycle, and triggered ERS in GC cells. Baicalein impeded the PI3K/AKT pathway by activating BTG3, thereby triggering ERS and inducing apoptosis. BTG3 inhibition reversed baicalein-induced apoptosis and ERS. Baicalein regulated GC cells in a concentration-dependent manner. Moreover, in xenograft mice, baicalein prevented tumor growth, decreased Ki67-positive cells, activated BTG3, and inhibited the PI3K/AKT pathway, thus activating ERS and increasing apoptotic cells. Conclusion Baicalein facilitates GC cell apoptosis by triggering ERS via repression of the PI3K/AKT pathway. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 2468-0842 |
| Relation: | https://doaj.org/toc/2468-0842 |
| DOI: | 10.1186/s13765-022-00759-x |
| URL الوصول: | https://doaj.org/article/9c3e9d07e5184457a9460b96700856a2 |
| رقم الأكسشن: | edsdoj.9c3e9d07e5184457a9460b96700856a2 |
| قاعدة البيانات: | Directory of Open Access Journals |
Find this article in full text from Springer Verlag. 
Full Text Finder | تدمد: | 24680842 |
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| DOI: | 10.1186/s13765-022-00759-x |