Retinoblastoma

XIST[LncRNA]

miR-142-5p[miRNA]

NA[mRNA]

RB cells

Homo sapiens (human)

Eur Rev Med Pharmacol Sci. 2020 Sep;24(18):9256-9264. doi: 10.26355/eurrev_202009_23007.

LncRNA XIST promotes proliferation and epithelial-mesenchymal transition of retinoblastoma cells through sponge action of miR-142-5p.

qRT-PCR;RIP assay;Western blot;Flow Cytometry assay;RNA pull-down;

OBJECTIVE: 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. PATIENTS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: Ptv1 can promote the proliferation, invasion, and EMT of RB cells by regulating miR-142-5p.