High PRELID1 expression promotes epithelial-mesenchymal transition in gastric cancer cells and is associated with poor prognosis.
10.12122/j.issn.1673-4254.2025.07.21
- Author:
Xuan WU
1
;
Jiamin FANG
1
;
Weiwei HAN
1
;
Lin CHEN
1
;
Jing SUN
1
;
Qili JIN
1
Author Information
1. Department of Laboratory, Second Affiliated Hospital of Bengbu Medical University, Bengbu 233080, China.
- Publication Type:Journal Article
- Keywords:
PI3K/AKT/mTOR;
PRELID1;
epithelial mesenchymal transition;
gastric cancer;
prognosis
- MeSH:
Humans;
Stomach Neoplasms/metabolism*;
Epithelial-Mesenchymal Transition;
Prognosis;
Cell Movement;
Cell Line, Tumor;
Male;
Female;
Middle Aged;
Signal Transduction;
Neoplasm Invasiveness;
Phosphatidylinositol 3-Kinases/metabolism*;
Proto-Oncogene Proteins c-akt/metabolism*
- From:
Journal of Southern Medical University
2025;45(7):1535-1542
- CountryChina
- Language:Chinese
-
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), G3-4 stages (P=0.001), T3-4 stages (P=0.001), and N2-3 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.
