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Licochalcone a Disrupted Mitochondrial Function to Promote Cuproptosis in Glioblastoma Through Regulating RAS/MAPK
Fengfeng Zhou1,2, Chenglin Li3, Fengyuan Che4
1Guangzhou University of Chinese Medicine, Guangzhou, Guangdong, China.
Applied Biochemistry and Biotechnology
|May 19, 2026
Summary
Licochalcone A triggers cuproptosis, a cell death pathway, in glioma cells by increasing copper accumulation and disrupting mitochondria. This compound shows potential as a therapeutic agent by inhibiting tumor growth via the RAS/ERK pathway.
Area of Science:
- Biochemistry
- Cell Biology
- Oncology
Background:
- Glioma is a primary brain tumor with limited treatment options.
- Cuproptosis, a copper-dependent cell death pathway, is emerging as a potential therapeutic target in cancer.
- Licochalcone A is a natural compound with potential anti-cancer properties.
Purpose of the Study:
- To investigate the effect of Licochalcone A on cuproptosis in glioma cells.
- To elucidate the underlying molecular mechanisms of Licochalcone A-induced cuproptosis.
- To evaluate the therapeutic potential of Licochalcone A in an in vivo glioma model.
Main Methods:
- Glioma cell lines (U87 MG, U251) were treated with Licochalcone A.
- Assays included immunofluorescence, transmission electron microscopy (TEM), mitochondrial membrane potential analysis, and ROS detection.
- In vivo studies utilized a nude mouse xenograft model.
- Western blotting and other biochemical assays were performed to analyze protein expression and pathway activation.
Main Results:
- Licochalcone A induced cuproptosis in a dose-dependent manner, increasing Cu²⁺ accumulation and pyruvic acid levels.
- Mitochondrial membrane potential was reduced, accompanied by mitochondrial swelling and cristae disruption.
- Licochalcone A downregulated FDX1 and LIAS protein expression and increased cellular ROS levels.
- The compound inhibited glioma cell proliferation and reduced tumor volume/weight in vivo.
- Mechanistically, Licochalcone A inactivated the RAS/ERK signaling pathway.
Conclusions:
- Licochalcone A effectively induces cuproptosis in glioma cells.
- The mechanism involves copper accumulation, mitochondrial dysfunction, and ROS generation.
- Licochalcone A inhibits glioma growth by inactivating the RAS/ERK pathway.
- Licochalcone A represents a promising therapeutic candidate for glioma treatment.
