LncRNA SNHG15 acts as a ceRNA to promote breast cancer progression through the miR-153-3p/KLF5 signal axis.

Increasingly evidence shows that the interaction between long non-coding RNAs (lncRNAs), microRNAs (miRNAs) and their downstream target genes plays a pivotal role in the onset and progression of tumors, emerging as a focal point in tumor research. This study sought to assess the biological function of lncRNA SNHG15 and investigate the underlying mechanisms involved in SNHG15/miR-153-3p/KLF5 signal axis in breast cancer (BC). The expressions of SNHG15, miR-153-3p and KLF5 in human BC tissues and cell lines were detected by quantitative real-time PCR and/or western blot. To investigate the biological functions of SNHG15, we knocked it down in BC cells and observed its effects both and . The underlying mechanisms of competitive endogenous RNA (ceRNA) between SNHG15 and miR-153-3p were elucidated through bioinformatics analysis, dual-luciferase reporter assays and rescue experiments. SNHG15 expression was notably elevated in BC tissues and cell lines. Knockdown of SNHG15 significantly reduced the ability of proliferation, migration and invasion in BC cells. miR-153-3p was a direct target of SNHG15, while miR-153-3p mediated the expression of KLF5 in BC cell lines. In addition, the effect of SNHG15 downregulation on the biological behavior of BC cells can be offset by the inhibition of miR-153-3p. Mechanically, SNHG15 may act as the ceRNA of miR-153-3p, thereby regulating the expression of its target gene KLF5. SNHG15 promotes proliferation and metastasis by sponging miR-153-3p and regulates KLF5 expression, suggesting that SNHG15 may be a potential biomarker and therapeutic target for BC.