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HERG1 K+ channels on the leukemic cells mediated angiogenesis in vitro
Authors:Huiyu Li  Dongmei Guo  Fang Zheng  Kaiwei Liang  Wenying Li  Shenghua Jie
Affiliation:1. Center for Stem Cell Research and Application, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, Hubei, China
Abstract:Human ether-a-go-go-related gene (HERG1) K+ channels are overexpressed in leukemia, which contributes to neoangiogenesis. The purpose of this study was to investigate the role of HERG1 K+ channels on leukemia angiogenesis. We cultured human umbilical vein endothelial cells (HUVECs) in conditioned media, which were derived from leukemic cells with or without E-4031, a HERG1 K+ channel special inhibitor. The HUVECs proliferation was measured using CCK-8 assay and migration by a Trans-well. Endothelial tube formation was investigated using Matrigel. Vascular endothelial growth factor (VEGF) levels were tested by ELISA and VEGF mRNA expression using RT-PCR. Our results revealed that blocking HERG1 K+ channels could inhibit leukemia-induced HUVECs proliferation, migration, and tube formation in vitro. The results suggested that HERG1 K+ channels could increase leukemia angiogenesis. Furthermore, blockage of HERG1 K+ channels could also decrease leukemic cells secreting VEGF and expressing VEGF mRNA. HERG1 K+ channels have a promoting effect on leukemia angiogenesis, and the possible mechanism may be that HERG1 K+ channels enhance VEGF expression. Thus, HERG1 K+ channel is a potential target of antiangiogenesis in leukemia.
Keywords:HERG1 K^+hannels  angiogenesis  human umbilical vein endothelial cells  leukemia  vascular endothelial growth factor (VEGF)
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