Role of RhoA in hypoxia-induced breast cancer cell VEGF secretion and proliferation, migration and tube formation of HUVECs.
- Author:
Ji MA
1
;
Qingli ZHAO
;
Hui REN
;
Wenchao LIU
;
Yan XUE
Author Information
- Publication Type:Journal Article
- MeSH: Breast Neoplasms; metabolism; pathology; Cell Hypoxia; Cell Line, Tumor; Cell Movement; Cell Proliferation; Female; Gene Knockdown Techniques; Human Umbilical Vein Endothelial Cells; cytology; secretion; Humans; Transfection; Vascular Endothelial Growth Factor A; secretion; rhoA GTP-Binding Protein; metabolism
- From: Journal of Southern Medical University 2012;32(6):784-788
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the role of RhoA in regulating vascular endothelial growth factor (VEGF) secretion level in breast cancer cells and in the proliferation, migration and tube formation of human umbilical vascular endothelial cells (HUVECs) under hypoxia.
METHODSEnzyme-linked immunosorbent assay was used to examine the effect of V14RhoA plasmid transfection-induced RhoA activation and RhoA knockdown on VEGF secretion level in breast cancer MCF-7 cells under hypoxic condition. A MCF-7/HUVEC co-culture model was established to assess the effect of the changes in RhoA expressions in MCF-7 cells on HUVEC proliferation, migration, and tube formation under hypoxia.
RESULTSUnder hypoxic condition, RhoA activation promoted VEGF secretion in MCF-7 cells, and RhoA knockdown inhibited VEGF secretion. In the co-culture model, RhoA activation in the MCF-7 cells enhanced HUVEC proliferation, migration, and tube formation, and RhoA knockdown inhibited these changes.
CONCLUSIONUnder hypoxic condition, RhoA indirectly influences HUVECs to affect tumor angiogenesis by regulating VEGF level in breast cancer cells.
