三阴性乳腺癌和非三阴性乳腺癌在诸多生物学特征上都存在着显著的差异，造成这种差异的具体机制尚不明确。前期预实验中我们通过对比不同三阴性和非三阴性乳腺癌细胞在谷氨酰胺剥夺情况下Ribosome Profiling-Seq数据的差异，发现大量的LncRNA都具有翻译产物，其中由MLLT4-AS1编码微肽XBP1SBM在两种不同类型乳腺癌细胞中表达存在显著差异；进一步研究显示该微肽可能参与了XBP1s蛋白的核质穿梭，促进了XBP1s在细胞核内的聚集，这将有助于三阴性乳腺癌血管生成。据此，我们假设通过翻译组学的方法锁定的MLLT4-AS1编码微肽XBP1SBM可以通过调控XBP1s细胞内分布的方式影响三阴性乳腺癌的发生发展。本项目拟在此基础上联合使用大样本分析、机制和功能研究的模式，以期系统的阐明该微肽的异常表达与三阴性乳腺癌特殊的生物学特征之间的关系，为三阴性乳腺癌的防治提供科学依据和手段。

Biologically, there are numerous significant difference between TNBC and non-TNBC. However, its underlying mechanism remains largely unclear. Interestingly, we found that many lncRNAs have translational ability by analyzed the data of ribosome profiling that generated by four breast cancer cell lines under glutamine starvation. In addition, we identified a micropeptide, XBP1SBM, which encoded by lncRNA MLLT4-AS1, differentially expressed between cell lines of TNBC and non-TNBC. Further research shows that XBP1SBM potentially involved in the progression of nuclear-cytoplasmic shuttling of XBP1s, which increased its nuclear enrichment, and promoted the angiogenesis of TNBC. Accordingly, we hypothesized that the micropeptide XBP1SBM encoded by lncRNA MLLT4-AS1, which we identified by ribosome profiling sequencing, may involve in the carcinogenesis and development of TNBC by regulating the subcellular localization of XBP1s. This project is aimed at illuminating the relationship between abnormally expressing of the micopeptide and specific biological characteristic of TNBC by combining large-scale sample research, mechanism investigation and functional discovery, and providing new scientific basis and treatment for the prevention and treatment of TNBC.