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Tumor cell entry receptors are cell surface molecules (primarily transmembrane proteins) highly expressed on cancer cells, which can facilitate the internalization of therapeutic agents, toxins, viruses, or nanoparticles. Common examples include growth factor and cytokine receptors (EGFR, IL4R), nutrient receptors (transferrin receptor), and dependence receptors. These receptors are central to signal transduction pathways that drive cell proliferation, migration, survival, and immune evasion in cancer. Their overexpression or altered function in tumors makes them attractive for targeted therapy, but off-tumor toxicity and biological redundancy pose therapeutic challenges[2][5][6][1]. The term “tumor cell entry receptors” is collective and should be replaced by specific receptor names for precision in research or clinical applications.
Direct inhibition of proliferative/survival signaling (e.g., kinase blockers) Targeted delivery of cytotoxic payloads, using receptor internalization for uptake (“Trojan horse” strategy) Modulation of immune response (some induce immune cell recruitment or alter local environment) Blockade of ligand binding and downstream effects Induction of receptor-mediated apoptosis (for certain dependence receptors)
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