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Peptidoglycan recognition protein 1 (PGLYRP1), widely known as Tag7 in the context of oncology, is a secreted protein of the innate immune system that exhibits potent anti-tumor activity. When overexpressed in autologous tumor cells, Tag7 acts as a therapeutic agent by forming a stable cytotoxic complex with the molecular chaperone Hsp70 (Sashchenko et al., 2004). This Tag7-Hsp70 complex specifically targets and binds to the Tumor Necrosis Factor Receptor 1 (TNFR1) on the surface of cancer cells, triggering intracellular signaling pathways that lead to apoptotic or necroptotic cell death (Dukhanina et al., 2015). Beyond direct cytotoxicity, the presence of Tag7 on tumor cells serves as a potent chemoattractant for cytotoxic T-lymphocytes and natural killer (NK) cells, thereby overcoming the immunosuppressive microenvironment of the tumor. This immune effector system strategy effectively turns the patient's own tumor cells into a personalized vaccine that stimulates a systemic and durable anti-tumor immune response. Clinical applications, particularly in melanoma, have utilized Tag7-modified autologous cells to induce regression of both primary and metastatic lesions by activating multiple arms of the immune system (Gnuchev et al., 2005).
Induction of tumor cell apoptosis through the formation of a cytotoxic complex with Hsp70 that activates the TNFR1 signaling pathway; stimulation of autologous immune effector cells against tumor antigens (Sashchenko et al., 2004; Dukhanina et al., 2015).
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