Open Access

ARTICLE

Apigenin inhibits cell migration through MAPK pathways in human bladder smooth muscle cells

QINGXIN LIU^1§ , XIANGGUI CHEN^2§, GUOLIN YANG¹ , XUEWEN MIN³ , AND MAOXIAN DENG^1,*

1. Department of Animal Biology, School of Husbandry and Veterinary Medicine, Jiangsu Polytechnic College of Agriculture and Forestry, Jurong, Jiangsu 212400, China
2. School of Bioengineering, Xihua University, Chengdu, Sichuan 610039, China
3. Department of Pathology, People’s Hospital of Jurong, Jurong, Jiangsu 212400, China
§ These authors contributed equally to this work.
* Address correspondence to: Maoxian Deng. Department of Animal Biology, School of Husbandry and Veterinary Medicine, Jiangsu Polytechnic College of Agriculture and Forestry, 3 Changjiang Road, Jurong, Jiangsu 212400, P.R.China. Fax: (+86-511) 87291036. E-mail: dengok@hotmail.com

BIOCELL 2011, 35(3), 71-80. https://doi.org/10.32604/biocell.2011.35.071

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.

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