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 in vitro and in vivo. 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 in vivo. 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.

中文翻译：

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BMF对Bax的置换以依赖miRNA的方式介导STARD13 3'UTR诱导的乳腺癌细胞凋亡。

促凋亡和抗凋亡基因表达程序的平衡支配着癌细胞的凋亡进程。我们以前证明了STARD13 3'UTR通过抑制上皮-间质转化（EMT）抑制了乳腺癌的转移。然而，STARD13 3'UTR在乳腺癌细胞凋亡中的作用仍然难以捉摸。在这里，我们确定了STARD13 3'UTR在体外和体内均可促进细胞凋亡。从机制上讲，STARD13 3'UTR充当BMF（Bcl-2修饰因子）的ceRNA，从而以miRNA依赖的方式增加BMF的表达。同时，STARD13 3'UTR增强了BMF / Bcl-2的相互作用，从而在乳腺癌细胞中释放Bax（Bcl-2相关X蛋白）。最后，我们在体内验证了STARD13和BMF之间的ceRNA关系。总的来说，这些发现表明，STARD13 3'UTR可以作为BMF的ceRNA来促进细胞凋亡，并将STARD13 3'UTR识别为乳腺癌细胞中的潜在治疗靶标。