Abstract
Mounting evidence suggests that lncRNAs can exert functions in cancer progression in multiple manners. In recent years, competing endogenous RNA (ceRNA) has been widely reported in human cancers as a lncRNA-dominant molecular pathway. The current study aimed at proving the role of lncRNA downregulated RNA in cancer (DRAIC) in breast cancer (BRCA) progression. To be specific, qRT-PCR assay was conducted to measure the expression of DRAIC and other downstream target genes. It was uncovered that DRAIC was expressed at a high level in BRCA cells. Functional analyses, including CCK-8, colony formation, and EdU assays demonstrated that DRAIC depletion suppressed BRCA cell proliferation. In addition, cell apoptosis was promoted due to DRAIC knockdown. The inhibitory effect of DRAIC reduction on BRCA cell migration and invasion was proven by transwell assays. Mechanistically, DRAIC was confirmed to predominantly distribute in the cytoplasm and could interact with miR-432-5p. In addition, stem-loop binding protein (SLBP) was verified to be a downstream target of miR-432-5p and was positively regulated by DRAIC. Taken together, DRAIC sponged miR-432-5p to enhance SLBP expression, by which malignant behaviors of BRCA cells were promoted. Our findings may help to provide a promising therapeutic target for BRCA patients.
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Acknowledgements
We want to thank our laboratory staff for their contributions.
Funding
This study was supported by Construction of biological sample bank and clinical diagnosis and treatment information database of breast cancer, 2016YFC0901304.
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SL, HJ and ZZ designed the study. SL, HJ and DW contributed to implementation of experiments. ZZ worked out also all technical details. DW was responsible for the numerical calculations. ZZ and DW analyzed the data. All authors participated in the discussion of the results and contributed to the final paper.
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Li, S., Jia, H., Zhang, Z. et al. DRAIC promotes growth of breast cancer by sponging miR-432-5p to upregulate SLBP. Cancer Gene Ther 29, 951–960 (2022). https://doi.org/10.1038/s41417-021-00388-4
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DOI: https://doi.org/10.1038/s41417-021-00388-4
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