Knockdown of lncRNA XIST inhibits retinoblastoma progression by modulating the miR-124/STAT3 axis

Long non-coding RNA (lncRNA) X-inactive specific transcript (XIST) was reportedly to be tightly associated with tumorigenesis and progression of multiple cancers. However, the expression, biological function, and action mechanisms of XIST in retinoblastoma (RB) are still unknown. Here, we found that XIST expression was upregulated in RB tissues and cell lines, and that increased XIST expression was positively associated with advanced cTNM stage (III-V) and late differentiation status. We also revealed that knockdown of XIST inhibited RB cell proliferation, promoted cell cycle at G1/G0 phase, and induced cell apoptosis. Mechanistically, XIST directly bound to microRNA (miR)-124 in RB cells. XIST mRNA expression was inversely correlated with miR-124 in RB tissues. Importantly, miR-124 inhibition partially reversed the effect on cell proliferation, cycle arrest and apoptosis by XIST knockdown mediated. In addition, XIST could regulate expression of signal transducer and activator of transcription 3(STAT3), a directly target of miR-124 in RB. These findings implied that XIST promoted RB progression partially by modulating the miR-124/STAT3 axis.