Uncovers arsenic-binding proteins in human lung carcinoma cells, suggesting new targets for drug discovery.
Manipulating intracellular protein degradation systems provides extraordinary opportunities to find targeting proteins critical for drug discovery, as exemplified by proteolysis-targeting chimeras (PROTACs). Here, using trivalent arsenical-PROTAC (As(III)-PROTAC) probes, we developed an in situ proteolysis strategy to uncover the As-binding proteomes. Combined with proteomic analysis, this strategy identified 135 downregulated proteins in A549 human lung carcinoma cells, providing a candidate list for seeking As-binding proteins. Bioinformatics analysis revealed that they were involved in multiple pathways, such as the tricarboxylic acid cycle, DNA replication, and DNA repair. Karyopherin subunit α-2 (KPNA2) and cyclin-dependent kinase 1 (CDK1) could play core roles in the context of protein interactions. Western blotting confirmed the downregulation of embryonic ectoderm development (EED) and phospholipase A-2-activating (PLAA) proteins after the probe treatment. A cellular thermal shift assay (CETSA) exhibited intracellular binding of iAsIII to EED and PLAA. This work demonstrates the development and application of PROTAC probes for screening of As-binding proteomes and establishes a methodological foundation for comprehending the biological effects induced by arsenicals.
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