FUT3-B3GNT3 interaction promotes pancreatic cancer progression and chemoresistance via NF-κB signaling mediated autophagy.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is prone to drug resistance and a role for fucosyltransferase 3 (FUT3) is increasingly recognized. The current study investigated the mechanisms by which FUT3 contributes to PDAC. FUT3 expression was analyzed via bioinformatics and validated by immunohistochemistry (IHC). RNA sequencing analysis identified significantly upregulated genes in Gemcitabine (Gem)-resistant cells of PDAC(ASPC-1/Gem). The IC50 values, proliferative capacity, invasive potential, and migratory behavior of ASPC-1/Gem cells were quantitatively assessed using using Cell Counting Kit-8 (CCK-8), 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), wound healing, and transwell assays, respectively. Subcellular localization and autophagy were analyzed by immunofluores

SUBMITTER: Jin L 

PROVIDER: S-EPMC12690808 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature