Abstract A51: Acacetin in inhibiting tumor growth and angiogenesis

التفاصيل البيبلوغرافية
العنوان: Abstract A51: Acacetin in inhibiting tumor growth and angiogenesis
المؤلفون: Lisa Jiang, Ling-Zhi Liu, Bing-Hua Jiang, Yi Jing, Xiue Jiang
المصدر: Cancer Prevention Research. 3:A51-A51
بيانات النشر: American Association for Cancer Research (AACR), 2010.
سنة النشر: 2010
مصطلحات موضوعية: Cancer Research, Acacetin, Angiogenesis, Biology, medicine.disease_cause, Molecular biology, Blot, Vascular endothelial growth factor, chemistry.chemical_compound, Chorioallantoic membrane, Oncology, chemistry, In vivo, Cancer research, medicine, Carcinogenesis, Protein kinase B
الوصف: Background: Acacetin (5,7-dihydroxy-4′-methoxyflavone) is a member of the flavonoid compound familys, some of which have anti-cancerous effects. Angiogenesis is a key process during carcinogenesis and tumor growth; however, but the effect and the mechanisms of acacetin on angiogenesis and tumor growth remain to be elucidated. Methods: In order to determine the effect of acacetin on the expression of vascular endothelial growth factor (VEGF) and HIF-1α expression, we tested VEGF expression by reporter assay and HIF-1α expression by Western blotting and RT-PCR assay. To test whether overexpression of active form of AKT increases HIF-1 expression, transient transfection was performed. Tumor angiogenesis and tumor formation in vivo were examined by chicken chorioallantoic membrane (CAM). Results: Acacetin decreased the steady level of VEGF mRNA under the normoxia and hypoxia conditions while inhibiting, and inhibited VEGF transcriptional activation. To further determine the potential mechanism of acacetin in inhibiting VEGF expression, we showed demonstrated that acacetin inhibited HIF-1α expression and AKT activation. Overexpression of HIF-1α or AKT abolished acacetin-decreasing VEGF transcriptional activation, indicating that AKT and HIF-1 are the essential downstream targets of acacetin for inhibiting VEGF expression in the cells. Moreover, acacetin significantly inhibited ovarian cancer cells-induced angiogenesis and tumor growth in vivo through inhibiting HIF-1α and VEGF expression. Acacetin inhibited HIF-1α protein expression through increasing its degradation and decreasing its stability, but did not alter HIF-1α mRNA levels. Conclusion: These results indicate that acacetin inhibits tumor agnigenensis and growth by blocking the AKT/HIF-1/VEGF pathway. It may be a useful natural compound for cancer prevention and treatment. Citation Information: Cancer Prev Res 2010;3(12 Suppl):A51.
تدمد: 1940-6215
1940-6207
URL الوصول: https://explore.openaire.eu/search/publication?articleId=doi_________::153645908ddcd73be73a893bae45d766
https://doi.org/10.1158/1940-6207.prev-10-a51
رقم الأكسشن: edsair.doi...........153645908ddcd73be73a893bae45d766
قاعدة البيانات: OpenAIRE