Open AccessEvodiamine inhibits vasculogenic mimicry in HCT116 cells by suppressing hypoxia-inducible factor 1-alpha-mediated angiogenesis
Author(s) -
Dongqiang Zeng,
Peng Zhou,
Rong Jiang,
Xiaopeng Li,
Shiying Huang,
Danyang Li,
Guoli Li,
Lisha Li,
Shuang Zhao,
Ling Hu,
Jianhua Ran,
Dilong Chen,
Yaping Wang,
Jing Li
Publication year - 2021
Publication title -
anti-cancer drugs
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.651
H-Index - 93
eISSN - 1473-5741
pISSN - 0959-4973
DOI - 10.1097/cad.0000000000001030
Subject(s) - vasculogenic mimicry , angiogenesis , mmp2 , mmp9 , cancer research , matrigel , cd31 , chemistry , vascular endothelial growth factor , blot , biology , microbiology and biotechnology , metastasis , downregulation and upregulation , cancer , vegf receptors , biochemistry , gene , genetics
Evodiamine (Evo), a quinazoline alkaloid and one of the most typical polycyclic heterocycles, is mainly isolated from Evodia rugulosa. Vasculogenic mimicry (VM) is a newly identified way of angiogenesis during tumor neovascularization, which is prevalent in a variety of highly invasive tumors. The purpose of this study was to investigate the effect and mechanism of Evo on VM in human colorectal cancer (CRC) cells. The number of VM structures was calculated by the three-dimensional culture of human CRC cells. Wound-healing was used to detect the migration of HCT116 cells. Gene expression was detected by reverse transcription-quantitative PCR assay. CD31/PAS staining was used to identify VM. Western blotting and immunofluorescence were used to detect protein levels. The results showed that Evo inhibited the migration of HCT116 cells, as well as the formation of VM. Furthermore, Evo reduced the expression of hypoxia-inducible factor 1-alpha (HIF-1α), VE-cadherin, VEGF, MMP2, and MMP9. In a model of subcutaneous xenotransplantation, Evo also inhibited tumor growth and VM formation. Our study demonstrates that Evo could inhibit VM in CRC cells HCT116 and reduce the expression of HIF-1α, VE-cadherin, VEGF, MMP2, and MMP9.