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Article Publish Status: FREE
Abstract Title:

Gambogic Acid Inhibits Wnt/β-catenin Signaling and Induces ER Stress-Mediated Apoptosis in Human Cholangiocarcinoma.

Abstract Source:

Asian Pac J Cancer Prev. 2021 Jun 1 ;22(6):1913-1920. Epub 2021 Jun 1. PMID: 34181351

Abstract Author(s):

Kanoknetr Suksen, Keatdamrong Janpipatkul, Somrudee Reabroi, Natthinee Anantachoke, Vichai Reutrakul, Arthit Chairoungdua, Natthakan Thongon, Kanit Bhukhai

Article Affiliation:

Kanoknetr Suksen

Abstract:

OBJECTIVE: Gambogic acid (GA) has been reported to induce apoptosis in cholangiocarcinoma (CCA) cell lines. However, the molecular mechanisms underlying its anti-cancer activity remain poorly understood. This study was aimed to investigate GA's effect on human CCA cell lines, KKU-M213 and HuCCA-1, and its associated mechanisms on Wnt/β-catenin signaling pathway.

METHODS: Cell viability, apoptosis, and cell cycle analysis were conducted by MTT and flow cytometry. The effect of GA mediated Wnt/β-catenin and ER stress were determined by luciferase-reporter assay, qRT-PCR, and western blot analysis.

RESULTS: GA exhibited potent cytotoxicity in CCA cells which was associated with significantly inhibited cell proliferation, promoted G1 arrest, and activated caspase 3 mediated-apoptosis. GA attenuatedβ-catenin transcriptional levels, decreased β-catenin protein, and suppressed the expression of c-Myc, a downstream target gene of Wnt/β-catenin signaling. GA activated genes involved in ER stress mechanism in KKU-M213 and enhanced CCA's sensitivity to gemcitabine.

CONCLUSION: Our findings reveal that the molecular mechanism underpinning anti-cancer effect of GA is partially mediated through the inhibition of Wnt/β-catenin signaling pathway and induction of ER stress induced-apoptosis. GA may serve as a promising therapeutic modality for amelioration of gemcitabine-induced toxicity in CCA.

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