CoCl2 increases the expression of hypoxic markers HIF‑1α, VEGF and CXCR4 in breast cancer MCF‑7 cells
- Qing Li
- Rong Ma
- Mei Zhang
Published online on: November 8, 2017
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.