Vitexin attenuates epithelial ovarian cancer cell viability and motility in vitro and carcinogenesis in vivo via p38 and ERK1/2 pathways related VEGFA
| Autor: | Zhifang Zhang, Fang Guo, Xinlei Guan, Xueying Zhang, Cai-Hong Hua, Shuzhen Zhao, Rui-Jie Hou |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
TUNEL assay Cell growth Vitexin General Medicine 03 medical and health sciences chemistry.chemical_compound Vascular endothelial growth factor A Ovarian tumor 030104 developmental biology 0302 clinical medicine chemistry In vivo Apoptosis 030220 oncology & carcinogenesis Cancer research Viability assay |
| Zdroj: | Annals of Translational Medicine. 8:1139-1139 |
| ISSN: | 2305-5847 2305-5839 |
| DOI: | 10.21037/atm-20-5586 |
| Popis: | Background Epithelial ovarian cancer (EOC) is the most common type of ovarian tumor, however, effective treatment does not currently exist for this condition. This study evaluated the role of vitexin in mitigating EOC both in vitro and in vivo. Method SKOV-3 cells were used for in vitro experimentation. Xenotransplantation mouse models were set up by subcutaneously injecting mice with SKOV-3 cells. CCK8 was used to screen the optimal dose in vitro. Cell proliferation, invasion, number of microtubule nodules and apoptosis were respectively detected by colony formation assay, transwell assay, microtubule formation assay and flow cytometry. TUNEL and immunohistochemistry were used to detect tissues apoptosis and VEGF content. Western blot assay was used to detect the expression of Ki67, caspase-3, VEGFA, VEGFR2, ERK1/2 and p38. Results In vitro experiment, compared with the control group, 10 µL of vitexin significantly reduced Ki67 levels and enhanced tumor cell apoptosis rate. Additionally, the colony forming rate, invasive cells per field, and number of nodes/HPF in vitexin treated group decreased dramatically. The result of western blot showed that levels of p-p38/p38 and p-ERK1/2/ERK1/2 also noticeably decreased. In vivo experiment, 40 mg/kg of vitexin significantly inhibited tumor growth. In addition, vitexin significantly enhanced the percentage of tissues apoptosis, which was accompanied by a decrease in the percentage of VEGF-positive cells. Conclusions Vitexin decreased the proliferation and invasion of SKOV-3 cells and noticeably reduced tumor growth. These findings suggest that vitexin could be a promising therapy for EOC. |
| Databáze: | OpenAIRE |
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