Schematic illustration of stress-induced CNS dysregulation driving OSCC tumorigenesis and progression. (IMAGE)
Caption
Schematic illustration of stress-induced CNS dysregulation driving OSCC tumorigenesis and progression. Chronic stress hijacks the HPB axis, leading to hypothalamic PVN activation, increased pituitary POMC expression, and aberrant α-MSH secretion. This neuroendocrine response increases bone marrow PMN-MDSC accumulation and upregulates CXCL13 in the TME, thereby promoting PMN-MDSC recruitment, suppressing CD8⁺ T cell infiltration, and enhancing M2 macrophage polarization. Together, these changes establish an immunosuppressive TME that accelerates OSCC progression and recurrence. Pharmacological MC5R inhibition with JNJ-10229570 disrupts this circuit, restores antitumor immunity, and enhances the efficacy of anti-PD-1 therapy.
Credit
International Journal of Oral Science
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