Long non-coding RNA XIST confers aggressive progression via miR-361-3p/STX17 in retinoblastoma cells.

OBJECTIVE

Retinoblastoma (RB) is a frequent intraocular tumor in children. Long-non-coding RNA X inactive specific transcript (XIST) has been reported to participate in the RB process, while its potential role remains largely unknown.

PATIENTS AND

METHODS

The expression patterns of XIST, microRNA (miR)-361-3p, and Syntaxin 17 (STX17) were determined using quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) assay. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT), flow cytometry, and transwell assays were employed to reckon cell viability, apoptosis, and mobility in RB cells, respectively. Besides, the levels of STX17 and autophagy-related proteins were detected utilizing Western blot. Dual-Luciferase reporter assay was implemented to evaluate the interaction between miR-361-3p and XIST or STX17, and the role of XIST in tumor growth was analyzed through xenograft tumor model.

RESULTS

The expression levels of XIST and STX17 were higher in RB tissues and cells, but miR-361-3p was downregulated. Loss of XIST was inversely connected with aggressive characteristics, showing as the curb of cell proliferation, migration, invasion, autophagy, and enhancement of apoptosis in RB cells. Also, the deficiency of XIST caused the decrease of tumor growth in vivo. Meanwhile, miR-361-3p inhibitor partially rescued XIST detection-mediated cell behaviors in vitro. Similarly, miR-361-3p mimic-mediated suppressive effect on aggressive phenotypes was abolished after overexpression of STX17 in RB cells. Mechanically, XIST was a sponge of miR-361-3p to regulate STX17.

CONCLUSIONS

XIST functioned as an oncogenic lncRNA via miR-361-3p/STX17 axis in the progression of RB, which might provide a promising theoretical basis for the clinical therapy of RB.