ASAP1 Promotes Cholangiocarcinoma Progression via Wnt/β-Catenin Pathway

Abstract

This study sought to identify the relationship between ADP-ribosylation factor GTpase-activating protein (ASAP1) expression and clinical outcomes in Cholangiocarcinoma (CC) patients. Quantitative real-time PCR (qRT-PCR), Western blotting, and immunohistochemistry were used to analyze the expression of ASAP1 in CC tissue samples and cell lines (IHC). The survival rate and clinicopathological characteristics were also examined. Cell counting kit-8 (CCK-8), colony formation, and 5-ethynyl-2′-deoxyuridine (EdU) assays were used to detect cell proliferation. Flow cytometry was used to assess the cell cycle. The terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) test and flow cytometry were used to identify cell apoptosis. Xenograft tumor development in living mice was reported. ASAP1 expression was increased and associated with a poor prognosis in CC tissue samples. The expression of ASAP1 was associated with the tumor’s histological grade and size in clinical specimens. In vitro and in vivo, knocking down ASAP1 expression resulted in decreased ASAP1 cell proliferation, inhibited cell cycle progression, and increased apoptosis. ASAP1 cholangiocarcinoma controls the Wnt/β-catenin pathway’s activity, encourages cell apoptosis, migration, and invasion in culture, and fosters tumor development in vivo. ASAP1 was crucial to the origin and growth of CC tumors, which could be a beneficial treatment target for CC.