Displacement of Bax by BMF Mediates STARD13 3′UTR-Induced Breast Cancer Cells Apoptosis in an miRNA-Depedent Manner

The balance of pro- and antiapoptotic gene expression programs dominates the apoptotic progress of cancer cells. We previously demonstrated that STARD13 3′UTR suppressed breast cancer metastasis via inhibiting epithelial-mesenchymal transition (EMT). However, the roles of STARD13 3′UTR in breast cancer apoptosis remain elusive. Here, we identified that STARD13 3′UTR promoted cell apoptosis <i>in vitro</i> and <i>in vivo</i>. Mechanistically, STARD13 3′UTR acted as a ceRNA for BMF (Bcl-2 modifying factor), thus increasing BMF expression in an miRNA-dependent manner. Meanwhile, STARD13 3′UTR enhanced the interaction of BMF/Bcl-2 to release Bax (Bcl-2 associated X protein) in breast cancer cells. Finally, we verified the ceRNA relationship between STARD13 and BMF <i>in vivo</i>. Collectively, these findings suggest that STARD13 3′UTR could act as a ceRNA for BMF to promote apoptosis and recognize STARD13 3′UTR as a potential therapeutic target in breast cancer cells

Recyclable Metallic Imidazolium-Based Ionic Liquid-Catalyzed Selective Mono- and Double-Hydroboration in Water

The recyclable metallic imidazolium-based ionic liquid-catalyzed mono-hydroboration of imines, double-hydroboration of imine with aldehyde, and double-hydroboration of aniline with glutaric dialdehyde in the presence of HBpin in water is described for the first time. The ionic liquid [BMIm][FeCl4] showed excellent activity, high selectivity, and good recyclability for the catalytic imine hydroborations. This catalytic system widely tolerated various functional rings and unsaturated groups without additional reduction. Furthermore, the metallic ionic liquid [BMIm][FeCl4] could be reused for more than 15 runs in water without decay of the catalytic activity

RNA Binding Protein RNPC1 Inhibits Breast Cancer Cell Metastasis via Activating STARD13-Correlated ceRNA Network

RNA binding proteins (RBPs) are pivotal post-transcriptional regulators. RNPC1, an RBP, acts as a tumor suppressor through binding and regulating the expression of target genes in cancer cells. This study disclosed that RNPC1 expression was positively correlated with breast cancer patients’ relapse-free and overall survival and that RNPC1 suppressed breast cancer cell metastasis. Mechanistically, RNPC1 promotes competing endogenous RNA (ceRNA) network crosstalk among STARD13, CDH5, HOXD10, and HOXD1 (STARD13-correlated ceRNA network), which we previously confirmed in breast cancer cells through stabilizing the transcripts and thus facilitating the expression of these four genes in breast cancer cells. Furthermore, RNPC1 overexpression restrained the promotion of STARD13, CDH5, HOXD10, and HOXD1 knockdown on cell metastasis. Notably, RNPC1 expression was positively correlated with CDH5, HOXD1, and HOXD10 expression in breast cancer tissues and attenuated adriamycin resistance. Taken together, these results identified that RNPC1 could inhibit breast cancer cell metastasis via promoting a STARD13-correlated ceRNA network