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

In this study, the authors clarified the biological function of RBM7 in breast cancer and investigated its potential molecular mechanism by identifying its key mRNA targets.

Data access: Datasets supporting Figures 1-6, Supplementary figures 1 and 2 are publicly available in the figshare repository as part of this data record ( The Cancer survival curve data are also publicly available in The Human Protein Atlas repository at: RNA sequencing data of RBM7 on global RBM7 gene regulation are publicly available in the NCBI Sequence Read Archive (SRA) repository at Full and Uncropped Western blots are available as part of the supplementary information (Supplementary figure 4).

Study approval: 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.

Study aims and methodology:
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.
In vitro, 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 in vivo 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 in vitro and in vivo, 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.

Datasets supporting figures and supplementary figures: 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.