[High PRELID1 expression promotes epithelial-mesenchymal transition in gastric cancer cells and is associated with poor prognosis].

Q3 Medicine

南方医科大学学报杂志 Pub Date : 2025-07-20 DOI:10.12122/j.issn.1673-4254.2025.07.21

Xuan Wu, Jiamin Fang, Weiwei Han, Lin Chen, Jing Sun, Qili Jin

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引用次数: 0

Abstract

Objectives: To investigate the correlation of PRELID1 with gastric cancer (GC) progression, prognosis, and epithelial-mesenchymal transition (EMT) and the underlying mechanisms.

Methods: We analyzed the data of 115 patients undergoing radical gastrectomy for GC in our hospital between February, 2018 and March, 2023 to explore the correlation of PRELID1 expression level in GC tissues with tumor progression and patient prognosis. In cultured GC cells, the effects of lentivirus-mediated overexpression or interference of PRELID1 were observed on cell migration, invasion and EMT.

Results: Immunohistochemical staining revealed significantly higher PRELID1 expression in GC tissues (P<0.001), whose expression level was positively correlated with CEA ≥5 ng/mL (P=0.007), CA199 ≥37 U/mL (P=0.007), G_3-4 stages (P=0.001), T_3-4 stages (P=0.001), and N_2-3 stages (P=0.020). Univariate and Cox multifactorial analysis showed that high PRELID1 level was an independent risk factor affecting 5-year survival of GC patients (P=0.001). In cultured GC cells, PRELID1 overexpression obviously promoted cell proliferation, migration, invasion, and the expressions of MMP2 and MMP9, and interference of PRELID1 produced the opposite changes. PRELID1 overexpression also increased the expressions of N-cadherin and vimentin and reduced the expression of E-cadherin. Mechanistic analyses showed that up-regulation of PRELID1 increased the expression of p-PI3K, p-AKT, and p-mTOR in GC cells, whereas its interference caused the opposite changes; the application of 740 Y-P, a PI3K/AKT pathway activator, significantly enhanced the migration, invasion, and EMT of GC cells with PRELID1 knockdown.

Conclusions: PRELID1 is highly expressed in GC and affects prognosis of the patients, and its high expression promotes migration, invasion and epithelial mesenchymal transition of GC cells possibly by activating the PI3K/AKT/mTOR pathway.

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[PRELID1高表达促进胃癌细胞上皮-间质转化，与预后不良相关]。

目的：探讨PRELID1与胃癌（GC）进展、预后、上皮-间质转化（EMT）的相关性及其机制。方法：对我院2018年2月至2023年3月行胃癌根治术的115例胃癌患者资料进行分析，探讨胃癌组织中PRELID1表达水平与肿瘤进展及患者预后的相关性。在培养的GC细胞中，观察慢病毒介导的PRELID1过表达或干扰对细胞迁移、侵袭和EMT的影响。结果：免疫组化染色显示，胃癌组织（PP=0.007）、CA199≥37 U/mL （P=0.007）、G3-4期（P=0.001）、T3-4期（P=0.001）、N2-3期（P=0.020）中PRELID1表达明显升高。单因素和Cox多因素分析显示，高PRELID1水平是影响GC患者5年生存率的独立危险因素（P=0.001）。在培养的GC细胞中，PRELID1过表达明显促进细胞增殖、迁移、侵袭，促进MMP2和MMP9的表达，而干扰PRELID1则产生相反的变化。PRELID1过表达使N-cadherin和vimentin的表达升高，E-cadherin的表达降低。机制分析表明，PRELID1的上调使GC细胞中p-PI3K、p-AKT和p-mTOR的表达增加，而其干扰则引起相反的变化；PI3K/AKT通路激活剂740 Y-P的应用显著增强了PRELID1敲低的GC细胞的迁移、侵袭和EMT。结论：PRELID1在胃癌中高表达并影响患者预后，其高表达可能通过激活PI3K/AKT/mTOR通路促进胃癌细胞迁移、侵袭及上皮间质转化。

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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