Abstract

The aim of the study was to investigate the effect of lncRNA XIST on the proliferation and epithelial-mesenchymal transition (EMT) of retinoblastoma (RB) and its relevant mechanism. 60 RB patients who were treated in our hospital were collected. The expression of XIST in tissues and cells was detected by qRT-PCR, and the effect of XIST on the prognosis of RB cells was observed. Stable and transient over-expression and suppression vectors were established and transfected into RB cells WERI-RB1 and Y79. CCK-8, transwell, and flow cytometry were used to evaluate the proliferation, invasion, and apoptosis of transfected cells. Western Blot was used to detect apoptosis-related proteins and EMT-related proteins. Dual-Luciferase report was used to determine the relationship between XIST and miR-142-5p. RNA pull-down and RIP experiments were used to determine the relationship between XIST and miR-142-5p. XIST was highly expressed in RB patients, which had a high diagnostic value. Patients with XIST high expression had a poor prognosis. After overexpression of XIST, the proliferation, invasion and EMT of cells increased, and apoptosis rate decreased, while inhibition of Ptv1 had the opposite effect. Dual-Luciferase report confirmed that XIST could target miR-142-5p. Functional analysis showed that the overexpression of miR-142-5p inhibited the proliferation, invasion and EMT of RB cells and promoted cell apoptosis. Rescue experiments showed that miR-142-5p could eliminate the inhibition of miR-142-5p on the proliferation, invasion, and EMT of RB cells by upregulating XIST expression. Ptv1 can promote the proliferation, invasion, and EMT of RB cells by regulating miR-142-5p.

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