Aberrant expression of LGALS3BP drives an unfavorable prognosis and more aggressive in HCC via regulating PI3K/AKT signaling.

Autor: Liu Y; Department of Postdoctoral Workstation, Liaocheng People's Hospital, Liaocheng, Shandong, China; Department of Mobile Post-Doctoral Stations, Shandong University, Jinan, Shandong, China; Department of Hepatobiliary Surgery, the Affiliated Taian City Central Hospital of Qingdao University, Taian, Shandong, China., Liang L; Department of Obstetrics and Gynecology, the Affiliated Taian City Central Hospital of Qingdao University, Taian, Shandong, China., Li J; Department of Breast Surgery, the Affiliated Taian City Central Hospital of Qingdao University, Taian, Shandong, China., Pang T; Department of Orthopaedics, the First People's Hospital of Taian City, Taian, Shandong, China., Zhang SH; Department of Obstetrics and Gynecology, the Affiliated Taian City Central Hospital of Qingdao University, Taian, Shandong, China., Xia ZY; Department of Neurology, Liaocheng People's Hospital and Liaocheng Clinical School of Shandong First Medical University, Liaocheng, Shandong, China. Electronic address: xiazhangyong2013@163.com.
Jazyk: angličtina
Zdroj: Tissue & cell [Tissue Cell] 2024 Aug; Vol. 89, pp. 102471. Date of Electronic Publication: 2024 Jul 10.
DOI: 10.1016/j.tice.2024.102471
Abstrakt: Lectin galactoside-binding soluble 3-binding protein (LGALS3BP) is associated with cancer metastasis and is a promising prognostic marker in neoplasms. In hepatocellular carcinoma (HCC), the prognostic impact and pro-metastatic function of LGALS3BP remain unclear. This study evaluated the endogenous LGALS3BP expression in HCC tissue and its association with prognosis. LGALS3BP protein levels were significantly elevated in clinical HCC tissues and cell lines. Increased LGALS3BP expression was closely associated with disease progression in HCC patients, and they also exhibited an unfavorable prognosis. Furthermore, the knockdown of LGALS3BP inhibited the growth, migration, and invasion of HCC cells in vitro. In mice xenografts, silencing LGALS3BP significantly inhibited tumor cell growth in vivo. Mechanically, upon LGALS3BP depletion, the tumor-suppressive function was dependent on inactivating Phosphatidylinositol 3-kinase (PI3K)/V-akt murine thymoma viral oncogene homolog (AKT) signaling pathway. Collectively, these findings suggest that LGALS3BP employs a pro-tumorigenic function in HCC and may be a promising HCC prognostic marker.
(Copyright © 2024. Published by Elsevier Ltd.)
Databáze: MEDLINE
Externí odkaz: