ArticleOncoTargets and therapy2026
Aloperine Induces Ferroptosis of Colorectal Cancer Cells via the Nrf2 Pathway.
Article in OncoTargets and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
2 citing papers in PubMed.
- Cholesterol-depleting nanozyme amplifies membrane-diffusive ferroptosis for potentiating anti-tumor immunity in colorectal cancer.Journal of materials science. Materials in medicine · 2026Article
- Natural products targeting the Nrf2 signaling pathway: potential targets and intervention strategies for the prevention and treatment of colorectal cancer.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: This study investigated the effects of ALO on apoptosis and ferroptosis in colorectal cancer HCT116 and SW480 cells and the underlying mechanisms. Methods: Cells were treated with varying ALO concentrations. CCK-8 assay assessed proliferation. Flow cytometry detected apoptosis. Lipid peroxidation was measured by BODIPY 581/591 C11 dye oxidation and TBA method. GSH content was determined by DTNB method. ROS and intracellular iron levels were assessed using fluorescent probes and iron assays. Molecular docking analyzed ALO-Nrf2 binding. Immunofluorescence detected Nrf2 expression. Western blot quantified apoptosis-related proteins (Bax, Bcl-2) and ferroptosis-related proteins (Nrf2, GPX4, xCT, DMT1). Effects of Nrf2 overexpression on ALO-treated cells were observed. Results: ALO inhibited cell viability and increased apoptosis dose-dependently. It elevated lipid peroxidation and intracellular iron while reducing GSH. Ferroptosis inhibitors DFO and Fer-1 reversed cell death and reduced apoptosis. ALO induced ROS production, upregulated Bax/Caspase3, and downregulated Bcl-2. Molecular docking suggested ALO binds to Nrf2 via hydrogen bonding. Immunofluorescence and Western blot showed ALO suppressed Nrf2, GPX4, xCT, and DMT1 expression concentration-dependently. Nrf2 overexpression significantly attenuated ALO's inhibitory effects on proliferation and its induction of ferroptosis and apoptosis. Conclusion: ALO suppresses colorectal cancer cell proliferation by inducing apoptosis and ferroptosis via inhibition of the Nrf2 signaling pathway.
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Registered trials
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