我们首次发现：lncRNA-RACGAP1P在乳腺癌细胞和组织中高表达且其与癌细胞侵袭和患者恶性进展正相关，更重要的是预实验显示lncRNA-RACGAP1P介导其真基因RacGAP1,引起Drp1磷酸化调控线粒体动态变化促进癌细胞侵袭/迁移。据预实验结果和生信分析，我们提出科学假说lncRNA-RACGAP1P通过miR-345-5p调控RacGAP1表达，激活MAPK通路/Drp1磷酸化调控癌细胞线粒体状态促进细胞侵袭转移。预实验结果和科学假说中关于lncRNA-RACGAP1P-真基因-线粒体动态变化之间的调控，及其与乳腺癌恶性表型关系等问题尚需深入研究，故我们拟用基因转染和CRISPR/Cas9技术构建的特定基因缺失细胞系等，经体内、外实验明确lncRNA-RACGAP1P介导真基因调控线粒体状态促进乳腺癌侵袭转移的作用和机制，为揭示lncRNAs在乳腺癌进展中发挥的功能提供依据。

Based on lncRNA expression profile assay and validation results, we discovered, for the first time, that lncRNA-RACGAP1P is expressed at a high level in breast carcinoma cells and breast carcinoma tissues, and its high expression positively correlates with malignant progression in breast carcinoma. Furthermore, more importantly, the our preliminary experiments show that lncRNA-RACGAP1P mediated the parent gene RacGAP1 can promote carcinoma cell invasion/migration through phosphorylation of Drp1 and modulating mitochondrial dynamics. Based on our preliminary experiments and analysis of bioinformatics, we deduce that lncRNA-RACGAP1P activates MAPK pathway/Drp1 phosphorylation via upregulating its parent gene RacGAP1 by competitively binding miR-345-5p, conseqently promotes mitochondrial fission and tumor invasion/metastasis. However, many questions still remain to be clarified, such as regulatory relationships among lncRNA-RACGAP1P, RacGAP1 and mitochondrial dynamics, and the relations of their expressions with malignant phenotypes of breast carcinoma. By means of different genes overexpression cells and CRISPER/Cas9-mediated specific gene-depleted cells (such as DICER-depleted cells, etc.), the in vitro and in vivo studies will be employed in this study in order to demonstrate the regulation mechanisms of lncRNA-RACGAP1P in promting breast carcinoma invasion/metastasis through modulating mitochondrial dynamics, therefore providing theoretical basis and experimental support for elucidating lncRNAs function in breast carcinoma progress.