Preclinical study reveals that bufalin directly drives EGFR endocytosis and lysosomal degradation in esophageal cancer, indicating a potential strategy to overcome tyrosine kinase inhibitor...
Esophageal squamous cell carcinoma (ESCC) stands out as a common cancer type worldwide, characterized by its notably high rates of occurrence and mortality. The epidermal growth factor receptor (EGFR) is one of the main targets for cancer treatment as it is one of the genes whose expression is often altered by overexpression, amplification, and mutation in a variety of solid tumors. Substantial efforts have been made to develop EGFR-targeted therapeutic agents, including monoclonal antibodies and tyrosine kinase inhibitors (TKIs). However, these agents exhibited limited efficacy due to the emergence of acquired resistance. Therefore, novel treatment strategies targeting EGFR are urgently needed. Recent studies have identified a few natural compounds that can efficiently inhibit EGFR, indicating that natural products may be potential sources for the development of new EGFR inhibitors. Here, using the Drug Affinity Responsive Target Stability (DARTS) assay combined with liquid chromatography/tandem mass spectrometry analysis, co-crystal method, we discovered that Bufalin directly interacts with EGFR and causes EGFR endocytosis and degradation in the lysosome. Moreover, Bufalin exhibits superior anti-tumor activity compared with another EGFR TKIs. Our study identified Bufalin as the first natural small-molecule EGFR degrader, which suppresses EGFR signaling by inducing the degradation of EGFR via the endosome-lysosome pathway.
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Tai et al. (2025) studied this question.
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