Icaritin-elevated circ_0000190 suppresses the malignant progression of multiple myeloma by targeting miR-301a

Icaritin has potential anticancer effects on various cancers, including multiple myeloma (MM). Recent studies claim that Icaritin can regulate the expression of noncoding RNAs (ncRNAs) in cancer development. This study aimed to investigate the role of circular RNA_0000190 (circ_0000190) and functional mechanism in Icaritin-treated MM. The expression of circ_0000190 and miR-301a was detected by quantitative real-time polymerase chain reaction. Cell cycle, apoptosis, migration, and invasion were investigated using flow cytometry assay, and transwell assay, respectively. The expression of BAX, BCL2, MMP2, and CCND1 was detected by western blot. The predicted target relationship between circ_0000190 and miR-301a was validated by dual-luciferase reporter assay and RNA immunoprecipitation assay. The activation of JAK1/STAT3 pathway was examined using western blot. Circ_0000190 was strikingly downregulated in MM specimens and cell lines, and Icaritin promoted the expression of circ_0000190. In function, circ_0000190 overexpression promoted MM cell cycle arrest and apoptosis but restrained the ability of migration and invasion. Icaritin blocked the development of MM by increasing circ_0000190 expression. MiR-301a was identified as a target of circ_0000190, and miR-301a reintroduction largely abolished the effects of circ_0000190 overexpression. The activation of JAK1/STAT3 pathway was promoted by miR-301a restoration. Icaritin played anticancer effects in MM partly by enhancing the expression of circ_0000190 and regulating the circ_0000190/miR-301a pathway. This study enhanced the understanding of the mechanism of Icaritin associated with circRNAs in MM.