@Article{biocell.2011.35.071,
AUTHOR = {QINGXIN LIU , XIANGGUI CHEN, GUOLIN YANG , XUEWEN MIN , AND MAOXIAN DENG},
TITLE = {Apigenin inhibits cell migration through MAPK pathways in human bladder smooth muscle cells},
JOURNAL = {BIOCELL},
VOLUME = {35},
YEAR = {2011},
NUMBER = {3},
PAGES = {71--80},
URL = {http://www.techscience.com/biocell/v35n3/37236},
ISSN = {1667-5746},
ABSTRACT = {Apigenin, a nonmutagenic flavonoid, has been shown to possess free radical scavenging activities, anticarcinogenic properties, antioxidant and anti-inflammatory effects. Recently, apigenin was reported
to cause gastric relaxation in murine. To assess possible effects of apigenin on migration of bladder smooth
muscle (SM) cell, we isolated SM cells from peri-cancer tissue of human bladder and established a cell model
that was capable to overexpress transiently MEKK1 (MEK kinase 1). Results showed that overexpression of
active human MEKK1 by adenoviruses infection induced migration of human bladder smooth muscle (hBSM)
cells and phosphorylation of MAPKs, ERK, JNK and p38, which are the downstream molecules of MEKK1.
Then, hBSM cell overexpressing MEKK1 were exposed to apigenin (50 μM). Our data indicated that apigenin inhibited significantly activation/phosphorylation of MAPKs and migration of hBSM cells induced by
MEKK1 overexpression. Besides, apigenin inhibited actin polymerization, which underlines muscle contraction and cell migration. The results suggest that apigenin inhibits activation of MAPKs and thereby the cell
migration. The mechanism might be that apigenin blocks signal transmission from MEKK1 to MAPKs.},
DOI = {10.32604/biocell.2011.35.071}
}