缺氧诱导因子讲义.docxVIP

12 Exercise training stimulates ischemia-induced neovascularization via phosphatidylinositol 3-kinase/Akt-dependent hypoxia-induced factor-1 alpha reactivation in mice of advanced age. 在老年小鼠中通过磷脂酰肌醇3激酶/Akt依赖的缺氧因子1α活化运动训练刺激缺血诱导的血管新生因子 18、Transcriptional regulation of BNIP3 by Sp3 in prostate cancer. BNIP3通过SP3在前列腺癌中的转录调控。 Keywords: prostate cancer;Sp3;BNIP3;transcriptional regulation;proliferation BACKGROUND The transcription factors Sp3/Sp1 are expressed in a various types of cancers and BNIP3 is overexpressed in prostate cancer. Although it has been demonstrated that BNIP3 is transcriptionally regulated by HIF-1α and is post-transcriptionally regulated by miR145, our previous data indicated that there might be some other transcription factors regulating BNIP3 in prostate cancer.This study is conducted to investigate whether BNIP3 expression is directly regulated by Sp3/Sp1 or not.转录因子SP1 SP3 /在各种类型的癌症和BNIP3的表达在前列腺癌中高表达。虽然它已被证明是αBNIP3 HIF-1的转录调节，后由miR145转录调控，我们以前的数据表明，可能有一些其他的转录调节因子在前列腺癌中的表达。本研究旨在探讨BNIP3的表达是由sp3 / SP1或不能直接调节 MATERIALS AND METHODS Bioinformatics analysis shows that BNIP3 promoter contains several potential Sp3/Sp1 binding sites. And then it is demonstrated that SP3 could regulate the BNIP3 transcriptionally by binding to the predicted sites by dual reporter gene assays, ChIP, and EMSA. The biological effects of SP3 regulating BNIP3 on prostate cancer cells proliferation are measured by MTT, TUNEL, and flow cytometry.生物信息学分析表明，BNIP3启动子包含了几个潜在的sp3 / Sp1结合位点。然后，它表明SP3可以调节转录结合BNIP3的预测双报告基因检测，芯片网站，EMSA。SP3调控BNIP3对前列腺癌细胞增殖的生物学效应是通过MTT法、TUNEL法和流式细胞仪检测。 RESULTS Our data show that Sp3 but not Sp1, is positively related to BNIP3 overexpression in prostate cancer.Sp3 can directly regulate BNIP3 transcription by mainly binding to the Sp3 binding sites (?624～?615 and ?350～?343) of BNIP3 promoter. Knockdown of Sp3 by RNA interference could reduce cells growth and lead to cells apoptosis in PC-3 and DU145. Sp3-dependent BNIP3 overexpression might be an important m