In vitro and in vivo apatinib inhibits vasculogenic mimicry in melanoma MUM-2B cells.

The effect of apatinib on the formation of vasculogenic mimicry (VM) was studied in a malignant melanoma cell line. MUM-2B cells cultured in three-dimensional Matrigel were treated with varying concentrations (0, 0.01, 0.05, 0.1, 0.5 μmol/L) of apatinib to test its effect on VM in vitro, followed by...

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Main Authors: Zong-Jun-Lin Liu, Yu-Juan Zhou, Rui-Lin Ding, Fang Xie, Shao-Zhi Fu, Jing-Bo Wu, Ling-Lin Yang, Qing-Lian Wen
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2018-01-01
Series:PLoS ONE
Online Access:http://europepmc.org/articles/PMC6063421?pdf=render
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author Zong-Jun-Lin Liu
Yu-Juan Zhou
Rui-Lin Ding
Fang Xie
Shao-Zhi Fu
Jing-Bo Wu
Ling-Lin Yang
Qing-Lian Wen
author_facet Zong-Jun-Lin Liu
Yu-Juan Zhou
Rui-Lin Ding
Fang Xie
Shao-Zhi Fu
Jing-Bo Wu
Ling-Lin Yang
Qing-Lian Wen
author_sort Zong-Jun-Lin Liu
collection DOAJ
description The effect of apatinib on the formation of vasculogenic mimicry (VM) was studied in a malignant melanoma cell line. MUM-2B cells cultured in three-dimensional Matrigel were treated with varying concentrations (0, 0.01, 0.05, 0.1, 0.5 μmol/L) of apatinib to test its effect on VM in vitro, followed by MTT proliferation and transwell invasion assays to determine the effect of apatinib on cell proliferation and invasion of MUM-2B cells. In vivo, we used a melanoma cancer model to test the effect of short-term apatinib (100, 200, 300 mg/kg) treatment on VM. Western blotting, immunohistochemistry staining, and CD31-PAS dual staining were performed to assess the expression of VEGFR-2, ERK-1/2, PI3K, and MMP-2, and formation of VM. The results showed apatinib-treated groups formed a lesser number of VM in 3D matrigel, while the cell viability in MTT proliferation assay and the number of migration cells in transwell invasion assay were significantly lower in apatinib-treated groups. In addition, short-term apatinib treatment inhibited angiogenesis, VM formation, and tumor growth in models of melanoma cancer. Mice in apatinib-treated groups showed a markedly reduced expression of VEGFR-2, ERK-1/2, PI3K, and MMP-2. In summary, apatinib could inhibit the expression of VEGFR-2, and downregulate the ERK1/2/PI3K/MMP-2 signaling cascade, which may be one of the underlying mechanisms by which apatinib inhibits angiogenesis and the development of VM in models of melanoma cancer, and restrains the formation of VM by MUM-2B cells. Apatinib shows inhibitory effects on cell proliferation and invasion of MUM-2B cells, which is a close relationship with the VM.
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spelling doaj.art-c5fed6df1d7c40db8cf104060717828b2022-12-21T18:56:55ZengPublic Library of Science (PLoS)PLoS ONE1932-62032018-01-01137e020084510.1371/journal.pone.0200845In vitro and in vivo apatinib inhibits vasculogenic mimicry in melanoma MUM-2B cells.Zong-Jun-Lin LiuYu-Juan ZhouRui-Lin DingFang XieShao-Zhi FuJing-Bo WuLing-Lin YangQing-Lian WenThe effect of apatinib on the formation of vasculogenic mimicry (VM) was studied in a malignant melanoma cell line. MUM-2B cells cultured in three-dimensional Matrigel were treated with varying concentrations (0, 0.01, 0.05, 0.1, 0.5 μmol/L) of apatinib to test its effect on VM in vitro, followed by MTT proliferation and transwell invasion assays to determine the effect of apatinib on cell proliferation and invasion of MUM-2B cells. In vivo, we used a melanoma cancer model to test the effect of short-term apatinib (100, 200, 300 mg/kg) treatment on VM. Western blotting, immunohistochemistry staining, and CD31-PAS dual staining were performed to assess the expression of VEGFR-2, ERK-1/2, PI3K, and MMP-2, and formation of VM. The results showed apatinib-treated groups formed a lesser number of VM in 3D matrigel, while the cell viability in MTT proliferation assay and the number of migration cells in transwell invasion assay were significantly lower in apatinib-treated groups. In addition, short-term apatinib treatment inhibited angiogenesis, VM formation, and tumor growth in models of melanoma cancer. Mice in apatinib-treated groups showed a markedly reduced expression of VEGFR-2, ERK-1/2, PI3K, and MMP-2. In summary, apatinib could inhibit the expression of VEGFR-2, and downregulate the ERK1/2/PI3K/MMP-2 signaling cascade, which may be one of the underlying mechanisms by which apatinib inhibits angiogenesis and the development of VM in models of melanoma cancer, and restrains the formation of VM by MUM-2B cells. Apatinib shows inhibitory effects on cell proliferation and invasion of MUM-2B cells, which is a close relationship with the VM.http://europepmc.org/articles/PMC6063421?pdf=render
spellingShingle Zong-Jun-Lin Liu
Yu-Juan Zhou
Rui-Lin Ding
Fang Xie
Shao-Zhi Fu
Jing-Bo Wu
Ling-Lin Yang
Qing-Lian Wen
In vitro and in vivo apatinib inhibits vasculogenic mimicry in melanoma MUM-2B cells.
PLoS ONE
title In vitro and in vivo apatinib inhibits vasculogenic mimicry in melanoma MUM-2B cells.
title_full In vitro and in vivo apatinib inhibits vasculogenic mimicry in melanoma MUM-2B cells.
title_fullStr In vitro and in vivo apatinib inhibits vasculogenic mimicry in melanoma MUM-2B cells.
title_full_unstemmed In vitro and in vivo apatinib inhibits vasculogenic mimicry in melanoma MUM-2B cells.
title_short In vitro and in vivo apatinib inhibits vasculogenic mimicry in melanoma MUM-2B cells.
title_sort in vitro and in vivo apatinib inhibits vasculogenic mimicry in melanoma mum 2b cells
url http://europepmc.org/articles/PMC6063421?pdf=render
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