Immune evasion signatures in oral squamous cell carcinoma: Differential TAP1–TAP2 expression by histological differentiation

Background: Transporter associated with antigen processing (TAP1 and TAP2) plays a key role in loading antigenic peptides onto MHC class I molecules, a critical step for initiating cytotoxic T-cell-mediated immunity. Disruptions in TAP function impair antigen presentation and promote tumor immune escape by limiting T-cell recognition. Understanding how TAP1 and TAP2 expression varies with tumor differentiation can clarify defects within the antigen-processing machinery (APM) and highlight their value as potential diagnostic or prognostic markers. Materials and Methods: A total of 52 tissue samples of oral squamous cell carcinoma (OSCC) cases were recruited, including well-differentiated OSCC ( n = 12), moderately differentiated OSCC ( n = 23), poorly differentiated OSCC ( n = 10), and suspected OSCC ( n = 7), and control healthy volunteer ( n = 41) groups. Total RNA was extracted from each tissue sample, and cDNA synthesis was done as per the standard protocols. Gene expression levels of TAP1 and TAP2 were quantified by SYBR green-based real-time polymerase chain reaction. Relative expression was evaluated using the 2 − ΔΔ Ct method, with suitable housekeeping gene controls. Fold-change values were compared across the histopathological grades to determine differentiation-specific variations. Results: TAP1 expression displayed a progressive increase with loss of differentiation. Compared with well-differentiated OSCC (1.25-fold), moderately differentiated (1.64-fold), and poorly differentiated tumors (2.03-fold) showed higher upregulation, suggesting enhanced dysregulation in advanced lesions. In contrast, TAP2 expression demonstrated an inverse trend. Suspected OSCC presented the highest TAP2 upregulation (2.35-fold), whereas poorly differentiated tumors showed the lowest expression (1.21-fold), representing a loss of TAP2 with tumor progression. Conclusion: TAP1 and TAP2 exhibit distinct and differentiation-dependent dysregulation patterns in OSCC. Increased TAP1 and diminished TAP2 expression in poorly differentiated tumors may reflect modified APM associated with tumor aggressiveness and immune evasion.