دورية أكاديمية
Brassicasterol inhibits hepatitis B virus-associated hepatocellular carcinoma development via suppression of AKT signaling pathway
| العنوان: | Brassicasterol inhibits hepatitis B virus-associated hepatocellular carcinoma development via suppression of AKT signaling pathway |
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| المؤلفون: | Jindi Zeng, Jiancheng Wu, Shuijiao Pang, Feifei Wang, Xin Yu, Shouhua Zhang, Junquan Zeng, Jinlong Yan, Jianping Lian |
| المصدر: | Infectious Agents and Cancer, Vol 18, Iss 1, Pp 1-9 (2023) |
| بيانات النشر: | BMC, 2023. |
| سنة النشر: | 2023 |
| المجموعة: | LCC:Neoplasms. Tumors. Oncology. Including cancer and carcinogens LCC:Infectious and parasitic diseases |
| مصطلحات موضوعية: | Brassicasterol, Hepatitis B virus, Inhibition, Hepatocellular carcinoma, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282, Infectious and parasitic diseases, RC109-216 |
| الوصف: | Abstract Background Hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC) does not respond well to current treatment options like sorafenib, and there is an urgent need for developing therapeutical strategies for HBV + HCC. Brassicasterol has previously shown anti-cancer and anti-viral activities, however, its value against HBV + HCC remains to be explored. Methods The inhibitory effect of brassicasterol and sorafenib was evaluated on HBV + HCC cell lines and xenograft mouse model. The cytotoxicity of brassicasterol on normal liver cells were measured by LDH assay. AKT agonist was used to identify the targeted signaling pathway by brassicasterol. Results Brassicasterol induced HBV + HCC cell death in a both dose-dependent and time-dependent manner, and such inhibition was more potent than sorafenib. Brassicasterol did not show apparent cytotoxicity to normal liver cells. Xenograft mouse model further confirmed the inhibitory effect of brassicasterol on the growth of HBV + HCC. Furthermore, signaling pathway analysis showed that brassicasterol-treated HBV + HCC cells had decreased level of phosphor-AKT expression while the addition of AKT agonist could counteract the inhibitory effect of brassicasterol on HCC, indicating that brassicasterol suppressed AKT pathway to exhibit anti-cancer activity in HBV + HCC cells. In addition, brassicasterol showed similar levels of inhibition on HBV− and HBV + HCC cells. Conclusion Brassicasterol possesses anti-cancer activity against HCC through the downregulation of AKT pathway and such activity is independent of HBV infection. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English |
| تدمد: | 1750-9378 |
| Relation: | https://doaj.org/toc/1750-9378 |
| DOI: | 10.1186/s13027-023-00502-1 |
| URL الوصول: | https://doaj.org/article/1afb4d8508054e599eee919ab4ae553b |
| رقم الأكسشن: | edsdoj.1afb4d8508054e599eee919ab4ae553b |
| قاعدة البيانات: | Directory of Open Access Journals |
Find this article in full text from Springer Verlag. 
Full Text Finder | تدمد: | 17509378 |
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| DOI: | 10.1186/s13027-023-00502-1 |