Bufalin and Anticancer Mechanisms in Traditional Medicine
Summary
Bufalin is a bufadienolide extracted from the dried skin secretion of toads (notably Bufo spp.) and has been employed for centuries in traditional Chinese medicine as the principal active constituent of Chansu and Huachansu. Modern research has revealed that bufalin exerts broad-spectrum anticancer effects by engaging multiple cellular pathways. It induces programmed cell death (apoptosis) and autophagy, suppresses proliferation, invasion and angiogenesis, and interferes with inflammatory signalling. At a molecular level, bufalin targets Na+/K+-ATPase, disrupts mitochondrial function, triggers reactive oxygen species production and modulates key signalling cascades such as PI3K/Akt/mTOR, Wnt/β-catenin, NF-κB and CAMKK2. Preclinical studies across diverse tumour types—including liver, biliary tract, lung, brain and bone cancers—have demonstrated significant antitumour activity in vitro and in vivo. While these findings underscore bufalin’s polypharmacology and its promise as a lead compound for novel anticancer agents, careful evaluation of its cardiotoxic potential and optimisation of delivery systems remain critical for clinical translation.
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Bufalin and Anticancer Mechanisms in Traditional Medicine publication trend
The graph below shows the total number of articles in bufalin and anticancer mechanisms in traditional medicine across all publications each year (not limited to Nature Index journals).
Technical terms
Apoptosis: Programmed cell death characterised by caspase activation and DNA fragmentation, essential for removal of tumour cells.
Autophagy: Intracellular degradation process that can promote or inhibit cancer cell survival by recycling cellular components.
Epithelial–mesenchymal transition (EMT): Phenotypic switch that enables epithelial cells to acquire migratory and invasive properties.
Mitochondrial dysfunction: Impairment of mitochondrial membrane potential and energy production, often leading to cell death.
Reactive oxygen species (ROS): Chemically reactive molecules derived from oxygen that can induce oxidative stress and trigger apoptosis.
Na+/K+-ATPase: Membrane enzyme that regulates ion gradients and can serve as a direct molecular target for bufalin.
References
- Bufalin targeting CAMKK2 inhibits the occurrence and development of intrahepatic cholangiocarcinoma through Wnt/β-catenin signal pathway. Journal of Translational Medicine (2023).
- Bufotalin Induces Oxidative Stress-Mediated Apoptosis by Blocking the ITGB4/FAK/ERK Pathway in Glioblastoma. Antioxidants (2024).
- New therapeutic aspects of steroidal cardiac glycosides: the anticancer properties of Huachansu and its main active constituent Bufalin. Cancer Cell International (2019).
- Bufalin suppresses hepatocellular carcinoma invasion and metastasis by targeting HIF-1α via the PI3K/AKT/mTOR pathway. Oncotarget (2016).
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