Apigenin inhibits endothelial-cell proliferation in G(2)/M phase whereas it stimulates smooth-muscle cells by inhibiting P21 and P27 expression.

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 Cancer

authors

Trochon V,Blot E,Cymbalista F,Engelmann C,Tang RP,Thomaïdis A,Vasse M,Soria J,Lu H,Soria C

doi

10.1002/(sici)1097-0215(20000301)85:5<691::aid-ijc

keywords:

subject

Has Abstract

pub_date

2000-03-01 00:00:00

pages

691-6

issue

5

eissn

0020-7136

issn

1097-0215

pii

10.1002/(SICI)1097-0215(20000301)85:5<691::AID-IJC

journal_volume

85

pub_type

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