SNHG16 promotes breast cancer progression by regulating the hsa-let-7b-5p/AURKA axis.

Background: Long non-coding RNAs (lncRNAs) play crucial roles in the progression of breast cancer (BC). The lncRNA small nuclear RNA host gene 16 (SNHG16), represents a lncRNA associated with tumor development. This study focuses on SNHG16 and its regulatory role in BC progression, validated through microarray analysis and in vitro experiments. Method: The GEO datasets GSE65194 and GSE61304 were used to identify differentially expressed lncRNAs, GSE41922 and GSE45666 for differentially expressed miRNAs, and GSE29431 and GSE42568 for differentially expressed mRNAs. The TCGA database was used to validate the genes identified in the previous analyses. The regulatory pathways of SNHG16 were identified through differential gene analysis, target gene prediction, functional enrichment analysis, and protein-protein interaction network analysis. RT-qPCR, Western blot, CCK-8, cell migration, and cell knockdown experiments were performed for validation. Results: Our study found that elevated expression levels of SNHG16 were associated with BC cell proliferation and poor prognosis. According to an in vitro knockdown assay, SNHG16 silencing inhibits the progression of BC. SNHG16 was found to positively regulate AURKA levels as a competitive sponge for hsa-let-7b-5p. Conclusion: The activity of the lncRNA SNHG16 can be triggered via the hsa-let-7b-5p/AURKA axes. These findings shed light on the novel molecular mechanisms underlying BC progression.