β-Asarone Inhibits Carboplatin Resistance in Retinoblastoma Cells Through the UCA1/miR-206/NRP1 Axis

Abstract

Retinoblastoma (RB) is an aggressive form of eye cancer. β-Asarone is a bioactive component isolated from the medicinal plant Acorus tatarinowii Schott and has anticancer effects on various human cancers. However, reports regarding the role of β-Asarone in RB remain limited. Our study investigates the mechanisms of β-Asarone in regulating drug resistance in RB, providing a theoretical foundation for RB treatment. A carboplatin-resistant RB cell line was established and treated with β-Asarone, followed by overexpression of long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1). The half-maximal inhibitory concentration and cell apoptosis were determined. The levels of lncRNA UCA1/miR-206/neuropilin 1 (NRP1) were measured. The subcellular localization of lncRNA UCA1 was examined. The binding relationships between lncRNA UCA1 and microRNA (miR)-206, and between miR-206 and NRP1 were analyzed. NRP1 expression was analyzed by Western blot assay. We found that β-Asarone downregulated lncRNA UCA1 expression in carboplatin-resistant RB cells. Overexpression of lncRNA UCA1 reversed the inhibitory effect of β-Asarone on cell drug resistance and cell proliferation and reduced apoptosis. LncRNA UCA1 functioned as a sponge for miR-206, which suppressed NRP1 expression. Inhibition of miR-206 or overexpression of NRP1 could partially reverse the suppressive effect of β-Asarone on RB cell drug resistance. In conclusion, β-Asarone suppresses RB cell drug resistance through the lncRNA UCA1/miR-206/NRP1 axis.

Keywords: NRP1; Retinoblastoma; lncRNA UCA1; miR-206; β-Asarone.