Abstract:
:Apigenin is a plant flavonoid that is thought to play a role in the prevention of carcinogenesis. However, its mechanism of action has not yet been elucidated. Because of the importance of angiogenesis in tumor growth, we investigated the effect of apigenin on endothelial and smooth-muscle cells in an in vitro model. Apigenin markedly inhibited the proliferation, and, to a lesser degree, the migration of endothelial cells, and capillary formation in vitro, independently of its inhibition of hyaluronidase activity. In contrast, it strongly stimulated vascular smooth-muscle-cell proliferation. The molecular mechanisms of apigenin activity were analyzed in these 2 types of cells. Our results show that apigenin inhibits endothelial-cell proliferation by blocking the cells in the G(2)/M phase as a result of the accumulation of the hyperphosphorylated form of the retinoblastoma protein. Apigenin stimulation of smooth-muscle cells was attributed to the reduced expression of 2 cyclin-dependent kinase inhibitors, p21 and p27, which negatively regulate the G(1)-phase cyclin-dependent kinase.
journal_name
Int J Cancerjournal_title
International journal of cancerauthors
Trochon V,Blot E,Cymbalista F,Engelmann C,Tang RP,Thomaïdis A,Vasse M,Soria J,Lu H,Soria Cdoi
10.1002/(sici)1097-0215(20000301)85:5<691::aid-ijckeywords:
subject
Has Abstractpub_date
2000-03-01 00:00:00pages
691-6issue
5eissn
0020-7136issn
1097-0215pii
10.1002/(SICI)1097-0215(20000301)85:5<691::AID-IJCjournal_volume
85pub_type
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