前列腺癌如何由雄激素依赖性（ADPC）临床进展为去势抵抗性（CRPC）、进而为神经内分泌性（NEPC），是目前前列腺癌研究的热点和难点。新近研究发现，N-Myc可能是前列腺癌尤其是NEPC的驱动基因，但其分子机制尚不清楚。我们前期研究结果显示，N-Myc可增进前列腺癌细胞多种恶性生物学行为，同时N-Myc可上调前列腺癌细胞中血管内皮标记物ANTXR1的表达。为此我们提出科学假说：N-Myc通过ANTXR1促进前列腺癌恶性进展。本研究拟从以下几方面论证该假说：①N-Myc通过ANTXR1促进前列腺癌新的血管生成；②N-Myc/ANTXR1调控前列腺癌的肿瘤生长、转移、神经内分泌转化；③N-Myc/ANTXR1影响前列腺癌雄激素去除治疗（ADT）、放射治疗（RT）的疗效。本研究将试图揭示N-Myc在前列腺癌恶性进展中的具体作用机制，为晚期前列腺癌的诊断和治疗提供新的靶点。

How prostate cancer clinically progressing from androgen-dependent (ADPC) to castration-resistance (CRPC), even to neuroendocrine prostate cancer (NEPC), is the focus of current prostate cancer research. Recent studies find that N-myc maybe the driver gene for prostate cancer, especially NEPC. However, the underlying molecular mechanisms are still unknown. Our preliminary study showed that N-Myc enhanced a variety of prostate cancer cell malignant biological behaviors; meanwhile N-myc increased the expression level of tumor endothelial marker ANTXR1 in prostate cancer cells. Therefore, we speculate that N-Myc promotes the malignant progression of prostate cancer by ANTXR1. To confirm the hypotheses, what we are going to prove are shown as follows. Firstly, N-Myc advances angiogenesis of prostate cancer by ANTXR1. Secondly, N-Myc/ANTXR1 regulates tumor growth, metastasis and neuroendocrine transformation of prostate cancer. Thirdly, N-Myc/ANTXR1 affects therapeutic effects of androgen deprivation therapy (ADT) and radiation therapy (RT). This study will provide us insights into the molecular mechanisms of N-Myc in the malignant progression of prostate cancer, and offer new targets for diagnosis and treatment of advanced prostate cancer.