What type of study is this?

This is a In Vitro Study study (also classified as: Animal Study).

September 30, 2025Open Access

Salinomycin promotes cell death via the activation of the ROS/NF-κB/NLRP3 pathway in cholangiocarcinoma

XZXianfei ZhouZhejiang International Studies University FYFan YangXijing Hospital YLYisheng LingTaizhou Municipal Hospital

Key Points

Salinomycin significantly increased cell death in cholangiocarcinoma cells via ROS/NF-κB/NLRP3 activation, indicating its therapeutic promise.
The treatment led to a dose-dependent rise in Annexin-V positive cells, with caspase-1 inhibition notably reducing this effect.
Salinomycin not only inhibited tumor growth in mice but also activated key pathways associated with cell death in tumor tissues.
These findings highlight salinomycin's potential as an effective treatment strategy against cholangiocarcinoma.

Abstract

Salinomycin (Sal), an ionophore antibiotic, has shown promising anti-cancer activity in multiple cancers. In this study, we aimed to investigate the effect of Sal on the ROS/NF-κB/NLRP3 pathway in cholangiocarcinoma (CCA) in vitro and in vivo. We observed that Sal inhibited cell proliferation, migration, and invasion. Sal promoted an increase of Annexin-V positive cells in Huh-28 and RBE cells in a dose-dependent manner, which was efficiently inhibited by VX-765 (Caspase-1 inhibitor), while Sal-induced increase of ROS levels was partially inhibited by exposure to N-acetyl-L-cysteine (ROS scavenger). Moreover, Sal inhibited tumor growth in RBE tumor-bearing mice. The activation of Sal on the ROS/NF-κB/NLRP3 pathway was also identified in CCA cells and tumor tissues. Collectively, these results suggested that Sal activated the ROS/NF-κB/NLRP3 pathway to promote pyroptosis-induced cell death in CCA and suggest it may be a promising treatment strategy for anti-CCA.

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