53BP1 是乳腺癌血管生成的一种新型调节因子。
53BP1 is a novel regulator of angiogenesis in breast cancer.
机构信息
Department of Breast Surgery, Qilu Hospital, Shandong University, Ji'nan, Shandong, China.
出版信息
Cancer Sci. 2013 Nov;104(11):1420-6. doi: 10.1111/cas.12247. Epub 2013 Sep 5.
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.
在我们之前的研究中，发现 53BP1 是一种肿瘤抑制因子，与乳腺癌的预后相关。然而，其在血管生成中的作用知之甚少。在本研究中，我们旨在揭示 53BP1 在乳腺癌血管生成中的作用。通过 RNA 干扰和异位表达策略来阐明 53BP1 在血管生成中的详细功能，我们观察到异位表达 53BP1 抑制细胞血管生成，53BP1 RNA 干扰导致体外和体内血管生成增加。在临床乳腺癌样本中，通过免疫组织化学分析发现 53BP1 与 CD31、MMP-2 和 MMP-9 呈负相关。此外，我们表明 Akt 通路参与了 53BP1 的抗血管生成功能。总的来说，我们的研究结果表明 53BP1 在抑制血管生成中起着至关重要的作用。这些发现表明 53BP1 可能为乳腺癌的靶向治疗提供了一种可行的方法。
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