53BP1 is a novel regulator of angiogenesis in breast cancer
Copyright policy )53BP1 is a novel regulator of angiogenesis in breast cancer
In our previous study, we found that 53BP1 was a tumor suppressor and was associated with prognosis in breast cancer. However, little is known about its role in angiogenesis. In the present study, we aimed to reveal the role of 53BP1 in angiogenesis of breast cancer. With RNA interference and ectopic expression strategies to elucidate the detailed function of 53BP1 in angiogenesis, we observed that ectopic expression of 53BP1 inhibited cellular angiogenesis and 53BP1 RNA interference led to an increase in angiogenesis both in vitro and in vivo. In clinical breast cancer samples, 53BP1 was inversely correlated with CD31, MMP‐2 and MMP‐9 by immunohistochemistry analysis. Furthermore, we showed that the Akt pathway was involved in the antiangiogenesis function of 53BP1. Overall, our findings demonstrate that 53BP1 plays a vital role in inhibiting angiogenesis. These findings suggest that 53BP1 might provide a viable target therapy for breast cancer.
- Qilu Hospital of Shandong University China (People's Republic of)
- Shandong Women’s University China (People's Republic of)
Neovascularization, Pathologic, Intracellular Signaling Peptides and Proteins, Breast Neoplasms, Chick Embryo, Platelet Endothelial Cell Adhesion Molecule-1, Mice, Matrix Metalloproteinase 9, Biomarkers, Tumor, Human Umbilical Vein Endothelial Cells, MCF-7 Cells, Animals, Matrix Metalloproteinase 2, Female, Neoplasm Invasiveness, Tumor Suppressor p53-Binding Protein 1, Proto-Oncogene Proteins c-akt, Signal Transduction
Neovascularization, Pathologic, Intracellular Signaling Peptides and Proteins, Breast Neoplasms, Chick Embryo, Platelet Endothelial Cell Adhesion Molecule-1, Mice, Matrix Metalloproteinase 9, Biomarkers, Tumor, Human Umbilical Vein Endothelial Cells, MCF-7 Cells, Animals, Matrix Metalloproteinase 2, Female, Neoplasm Invasiveness, Tumor Suppressor p53-Binding Protein 1, Proto-Oncogene Proteins c-akt, Signal Transduction
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