Abstract
Scoparone (SCO) is a compound found in the stems and leaves of Artemisia capillaris. The pharmacological uses of SCO include significant hypotensive, cholagogic, anti-inflammatory, analgesic, lipid-lowering, anti-asthmatic and anti-coagulant effects. The present study aimed to verify the anticancer potential of SCO in breast cancer (BC) cells and its underlying molecular mechanism. Cell Counting Kit-8 and flow cytometry were used to analyze the effects of SCO on cell viability and apoptosis. Nucleocytoplasmic separation was used to analyze the location of the long non-coding RNA (lncRNA) small nucleolar RNA host gene 12 (SNHG12) in BC cells. Reverse transcription-quantitative PCR was used to analyze the effect of SCO on the expression levels of SNHG12, microRNA (miRNA/miR)-140-3p and tumor necrosis factor receptor associated factor 2 (TRAF2). Western blotting was used to analyze the protein expression levels of TRAF2 and downstream nuclear factor κB (NF-κB) signaling pathways. The results demonstrated that SCO had a time- and dose-dependent inhibitory effect on the viability of BC cells, and that the upregulated lncRNA SNHG12 in BC cells was inhibited by SCO. SNHG12, which was primarily expressed in the cytoplasm, acted as a competing endogenous RNA, sponged miR-140-3p and inhibited the expression of miR-140-3p. The transcriptional activity and translational level of TRAF2, a downstream target of miR-140-3p, decreased following the SCO-mediated suppression of SNHG12 expression. As an upstream effector, TRAF2 activity reduction mediated the inhibition of NF-κB signaling, decreased the viability and migration of BC cells, and promoted BC cell apoptosis. In conclusion, SCO-induced inhibition of viability and promotion of apoptosis in BC cells are achieved through the inhibition of NF-κB signaling, which is associated with regulation of the SNHG12/miR-140-3p/TRAF2 axis. This understanding provides new drug candidates for the treatment of BC and a theoretical basis for biology.