肿瘤微环境诱导的内质网应激与肿瘤的生长和转移密切相关。本课题前期实验分别在内质网应激模型和高、低转移性细胞模型中，通过蛋白质组学技术筛选到内质网应激过程中被激活的BCAP31蛋白，预试验证实BCAP31能够显著促进乳腺癌转移。本课题拟在前期工作基础上，采用细胞、动物及临床标本等实验进一步明确BCAP31在乳腺肿瘤转移中的作用；采用IP-mass、RNA-seq、基因芯片等技术揭示BCAP31作用的靶基因及其调控乳腺癌转移的具体机制；采用生物信息学、报告基因、ChIP等技术揭示内质网应激上调BCAP31表达的机制；确定BCAP31在乳腺癌诊治中的临床意义，探索BCAP31上下游信号通路与乳腺癌类型、淋巴结转移、病人生存率等指标之间的临床规律。本课题有助于全面揭示BCAP31的转录激活及其促进乳腺癌转移的分子机制，有助于发现乳腺癌转移过程中新的分子靶点，对于指导临床治疗乳腺癌具有实际的应用价值

ER stress induced by tumor microenvironment, marked with low oxygen, nutrients deprivation and protein synthesis disorders, plays a critical role in tumor development and metastasis. Previously, by proteomic technology we found that expression of BCAP31 was upregulated both in breast cancer cells under ER stress and in highly metastatic breast cancer cells. Furthermore, overexpression of BCAP31 were preliminarily proved to promote breast cancer metastasis. In present study, the effect of BCAP31 on breast cancer metastasis will be further studied by cellular assays, animal experiments and clinical investigation. Mechanisms of BCAP31 promoting breast cancer metastasis will be further investigated by IP-mass, RNA-seq and gene array. Additionally, dysregulation of its upstream signaling by ER stress will be explored through ChIP assay, luciferase reporter gene assay and bioinformatics. Moreover, Diagnostic and therapeutical role of BCAP31 in breast cancer will be evaluated. The prognosis value of BCAP31 expression in breast cancer and its association with subtypes of breast cancer, lymph node metastasis and survival rate will be studied. Overall, our study will address the mechanisms underlie the dysregulation of BCAP31 and its role in breast cancer metastasis, uncover novel molecular targets to prevent breast cancer metastasis, and establish a practical role in guiding clinical treatment in breast cancer.