Data supporting the figures and supplementary figures and tables in the published article: Oncogenic action of the exosome cofactor RBM7 by stabilization of CDK1 mRNA in breast cancer

<b>Summary</b>This metadata record provides details of the data supporting the claims of the related manuscript: "Oncogenic action of the exosome cofactor RBM7 by stabilization of CDK1 mRNA in breast cancer". In the related study, the authors clarified the biological function of RBM7 in breast cancer and investigated its potential molecular mechanism by identifying its key mRNA targets.<br><br> <b>Data access</b>Datasets supporting Figures 1-6, Supplementary figures 1 and 2 are publicly available in the <i>figshare </i>repository as part of this data record.The Cancer survival curve data are also publicly available in <i>The Human Protein Atlas</i> repository at: https://identifiers.org/hpa:ENSG00000076053.RNA sequencing data of RBM7 on global RBM7 gene regulation are publicly available in the <i>NCBI Sequence Read Archive (SRA) </i>repository at https://identifiers.org/ncbi/insdc.sra:SRP274505. Full and Uncropped Western blots are available as part of the Supplementary Material (Supplementary figure 4).<br><b>Study approval</b>All samples were collected according to the ethics of Dec-Helsinki's mourning and were approved by the First Affiliated Hospital Research Committee of Nanjing Medical University. The Institutional Animal Care and Use Committee of Nanjing Medical University approved these animal studies, which were consistent with the National Institutes of Health (NIH) care and use of Laboratory Animals guide. <br><br><b>Study aims and methodology</b>RNA exosome can target the specific RNAs for their processing/degradation by distinct exosome cofactors. As a key component in exosome cofactors, RNA binding motif protein 7 (RBM7) shows the binding specificity for uridine-rich sequences in mRNAs via its RNA recognition motifs. However, the specific function of RBM7 in human breast cancer remains unclear. <i>In vitro</i>, experiments revealed that knockdown of RBM7 dramatically inhibited breast cancer cell proliferation, while inducing G1 cell cycle arrest; the opposite was true when RBM7 was overexpressed. Meanwhile, experiments <i>in vivo</i> confirmed the oncogenic function of RBM7 in breast cancer. RNA sequencing and the following pathway analysis found that cyclin-dependent kinase1 (CDK1) was one of the main gene regulated by RBM7. Overexpression of RBM7 increased CDK1 expression, while RBM7 knockdown decreased it. RIP assays additionally found that RBM7 bound directly to CDK1 mRNA. It was also found that RBM7 could directly bind to the AU-rich elements (AREs) in 3′-UTR of CDK1 mRNA, which contributed to the stability of CDK1 mRNA by lengthening its half-life. More importantly, the oncogenic activity reduced by knockdown of RBM7 could be rescued by overexpression of CDK1 both <i>in vitro</i> and <i>in vivo</i>, but mutant CDK1 failed. All the evidences implied RBM7 promoted breast cancer cell proliferation by stabilizing CDK1 mRNA via binding to AREs in its 3′-UTR. As we knew, it was the first attempt to connect the RNA exosome to the tumor development, providing new insights into the mechanisms of RNA exosome-linked diseases.<br><b>Datasets supporting figures and supplementary figures</b>Research Data Support datasummary form.xlsx is in .xlsx file format and describes all the datasets (names, dataset format and links to datasets) supporting the figures and supplementary figures in the published article.<br>

<b>摘要</b>本元数据记录详细阐述了支撑相关论文《外切体辅助因子RBM7通过稳定CDK1 mRNA在乳腺癌中的致癌作用》相关结论的实验数据。在本研究中，作者明确了RBM7在乳腺癌中的生物学功能，并通过鉴定其关键mRNA靶标，探究了其潜在分子机制。<br><br> <b>数据获取</b>支撑图1至图6、补充图1及补充图2的数据集已作为本数据记录的一部分，公开收录于<i>figshare</i>仓储。癌症生存曲线数据亦公开收录于<i>人类蛋白质图谱（The Human Protein Atlas）</i>仓储，链接为：https://identifiers.org/hpa:ENSG00000076053。RBM7全基因组基因调控相关的RNA测序数据，公开收录于<i>美国国家生物技术信息中心序列读取存档（NCBI Sequence Read Archive, SRA）</i>仓储，链接为：https://identifiers.org/ncbi/insdc.sra:SRP274505。完整未裁剪的蛋白质免疫印迹（Western blots）作为补充材料的一部分（对应补充图4）。<br><b>研究伦理审批</b>所有样本的采集遵循赫尔辛基宣言（Declaration of Helsinki）伦理准则，并经南京医科大学第一附属医院伦理委员会批准。本动物实验经南京医科大学实验动物管理与使用委员会（Institutional Animal Care and Use Committee）审核通过，符合美国国立卫生研究院（National Institutes of Health, NIH）《实验动物护理与使用指南》。<br><br><b>研究目的与方法</b>RNA外切体（RNA exosome）可通过不同的外切体辅助因子靶向特定RNA进行加工或降解。作为外切体辅助因子的关键组分RNA结合基序蛋白7（RBM7）可通过其RNA识别基序（RNA recognition motifs），对mRNA中富含尿苷的序列具有结合特异性。然而，RBM7在人类乳腺癌中的具体功能仍未明确。<i>体外（In vitro）</i>实验显示，敲低RBM7可显著抑制乳腺癌细胞增殖，并诱导G1期细胞周期阻滞；而过表达RBM7则呈现相反效果。同时，<i>体内（In vivo）</i>实验证实了RBM7在乳腺癌中的致癌功能。RNA测序及后续通路分析发现，细胞周期蛋白依赖性激酶1（CDK1）是RBM7调控的核心基因之一。过表达RBM7可上调CDK1的表达，而敲低RBM7则下调其表达。RNA免疫沉淀实验（RIP assays）进一步证实，RBM7可直接结合CDK1 mRNA。研究还发现，RBM7可直接结合CDK1 mRNA 3'非翻译区（3′-UTR）中的富AU元件（AU-rich elements, AREs），通过延长其半衰期以增强CDK1 mRNA的稳定性。更为重要的是，<i>体外（In vitro）</i>及<i>体内（In vivo）</i>实验中，敲低RBM7所降低的致癌活性，可通过过表达野生型CDK1得以挽救，但突变型CDK1则无法实现上述挽救。所有实验证据表明，RBM7可通过结合CDK1 mRNA 3′-UTR中的富AU元件以稳定CDK1 mRNA，进而促进乳腺癌细胞增殖。据我们所知，本研究首次将RNA外切体与肿瘤发生相关联，为RNA外切体相关疾病的机制研究提供了全新视角。<br><b>支撑图表及补充图的数据集</b>Research Data Support datasummary form.xlsx为.xlsx格式文件，用于描述支撑已发表论文中所有图表及补充图的数据集（包括数据集名称、格式及数据集链接）。