敲除 PRDX2 可抑制体外培养的尤文氏肉瘤细胞的增殖、生长、迁移、侵袭和 MMP9 活性。

IF 1.9 Q4 ONCOLOGY Cancer reports Pub Date : 2024-09-05 DOI:10.1002/cnr2.2122

Ruifeng Xue, Zhengfu Fan, Yunhe An

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摘要

背景：尤文氏肉瘤（ES）是儿童和青少年中第二常见的恶性原发性骨肿瘤。目的：在此，我们研究了PRDX2在ES发病中的作用和机制：通过特异性 siRNA 干扰（si-PRDX2）敲除 A673 和 RDES 细胞中 PRDX2 的表达。si-PRDX2 能显著抑制 Akt 的磷酸化和细胞周期蛋白 D1 的表达。利用JASPAR和UCSC数据库预测了可能调控PRDX2转录的转录因子，并利用双荧光素酶和染色质共免疫沉淀实验进行了分析。SNAI1可通过与预测的启动子结合位点结合来激活PRDX2的转录：结论：PRDX2可能是ES的潜在治疗靶点。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Knockdown of PRDX2 Inhibits the Proliferation, Growth, Migration, Invasion, and MMP9 Activity of Ewing's Sarcoma Cells Cultured In Vitro

Background

Ewing’s sarcoma (ES) is the second most common malignant primary bone tumor in children and adolescents. Peroxiredoxin 2 (PRDX2) is an antioxidant enzyme.

Aims

Here, we investigated the role and mechanism of PRDX2 in the development of ES.

Methods and results

PRDX2 expression was knocked down in A673 and RDES cells by specific siRNA interference (si-PRDX2). Knockdown of PRDX2 strongly inhibited the proliferation, growth, migration, invasion, and MMP9 activity and induces apoptosis of A673 and RDES cells. si-PRDX2 significantly inhibited the phosphorylation of Akt and the expression of cyclin D1. The transcription factor that might regulate PRDX2 transcription was predicted with the JASPAR and UCSC databases, and analyzed using dual-luciferase and Chromatin co-immunoprecipitation experiments. SNAI1 could activate the transcription of PRDX2 by binding to predicted promoter binding site.