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.
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Competitive endogenous messenger RNA (ceRNA) affects transcription of other RNA molecules by competitively binding common microRNAs. Previous studies have shown that TP53INP1 functions as a suppressor in tumor metastasis. Our study elucidated StarD13 messenger RNA as a ceRNA in regulating migration and invasion of breast cancer cells.
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