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LRG1 Is Involved in the Progression of Ovarian Cancer via Modulating FAK/AKT Signaling Pathway

Authors :
Dongling Wu
Weiwei Xie
Xin Chen
Huizhen Sun
Source :
Frontiers in Bioscience-Landmark, Vol 28, Iss 5, p 101 (2023)
Publication Year :
2023
Publisher :
IMR Press, 2023.

Abstract

Background: Rapid progression and early metastasis remain the main cause of high mortality in epithelial ovarian cancer (EOC) patients. The objective of this study was to explore the mechanisms of EOC progression and detect the function of leucine-rich alpha-2-glycoprotein 1 (LRG1) in modulating the pathologic process. Methods: Ultracentrifugation was initially performed to extract exosomes from the urine samples of EOC patients and healthy female subjects. Mass spectrometry (MS) was employed to analyze differentially expressed proteins. Survival analysis was performed to examine the association between LRG1 levels and the prognosis of EOC patients. LRG1 silencing ovarian cancer cell lines were built and cell migration was further evaluated via wound healing and transwell assays. Immunoblot, immunofluorescence and immunohistochemistry analyses were performed. A subcutaneous tumor model was established to study the function of LRG1 in vivo. Results: Exosomal LRG1 was specifically expressed in urine samples of EOC patients and high LRG1 levels were significantly associated with poor prognosis. Function analyses showed that LRG1 was associated with ovarian cancer migration and progression. Mechanistically, LRG1 was significantly related to the focal adhesion kinase/protein kinase B (FAK/AKT) signaling pathway. Conclusions: LRG1 participated in progression and metastasis of ovarian cancer via activation of the FAK/AKT pathway probably.

Details

Language :
English
ISSN :
27686701
Volume :
28
Issue :
5
Database :
Directory of Open Access Journals
Journal :
Frontiers in Bioscience-Landmark
Publication Type :
Academic Journal
Accession number :
edsdoj.59d1497265bc4c6980950cf38e559c56
Document Type :
article
Full Text :
https://doi.org/10.31083/j.fbl2805101