CoCl2 increases the expression of hypoxic markers HIF-1α, VEGF and CXCR4 in breast cancer MCF-7 cells.

Abstract

The aim of the present study was to investigate the effect of a hypoxic environment on the biological behavior of breast cancer MCF-7 cells, using CoCl2 to mimic the hypoxia model in breast cancer cells. Using 50, 100, 150 and 200 µM CoCl2 as a hypoxic inducer, a hypoxic model was established in MCF-7 cells in vitro. MTT, reverse transcription-quantitative polymerase chain reaction (RT-qPCR), terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) and western blotting assays were performed to detect MCF-7 cell proliferation under hypoxic conditions and the expression of the hypoxic markers hypoxia-inducible factor-1α (HIF-1α), vascular endothelial growth factor (VEGF) and C-X-C motif chemokine receptor 4 (CXCR4) mRNA and that of the associated proteins. The RT-qPCR results revealed that there were no obvious changes in the expression of HIF-1α mRNA; however, the expression of CXCR4 and VEGF mRNA increased significantly following treatment with different CoCl2 concentrations (P<0.05). The results of western blotting identified that CoCl2 significantly induced the expression of HIF-1α, CXCR4 and VEGF proteins (P<0.05). The MTT assay revealed that different concentrations of CoCl2 inhibited the proliferation of MCF-7 cells. The TUNEL assay demonstrated that CoCl2 was able to trigger apoptosis of MCF-7 cells. Therefore, the results of the present study identified that CoCl2 is able to control MCF-7 cell proliferation and apoptosis, also increasing the expression of HIF-1α, CXCR4 and VEGF. The present study may aid the discovery of a novel method to prevent cell damage and decrease cell proliferation in order to prevent the occurrence and development of breast cancer.