Identification of TAP2 as a novel immune target in human cancers: insights from integrated bioinformatics and experimental approaches.

Background: Transporter 2, ATP binding cassette (ABC) subfamily B member (TAP2), encodes a protein within the ABC transporter superfamily. TAP2 plays a role in the progression of cancers, such as cervical, breast, and lung cancers. However, the relationship between TAP2 and cancer prognosis, immune cell infiltration, tumor microenvironment, and immunotherapy remains unexplored. Therefore, this study aims to investigate the effect of TAP2 expression on its role in predicting tumor prognosis and immunotherapy efficacy.

Methods: Bioinformatics analyses such as Gene Set Enrichment Analysis, single-cell, and Connectivity Map analyses were used to comprehensively assess TAP2-related genomic alterations, prognostic value, enrichment pathways, single-cell expression patterns, and potential targeting inhibitors. In addition, molecular docking techniques were used to simulate drug binding to TAP2. WB and RT-qPCR were used to detect differences in TAP2 expression in glioma cell lines. The U251MG cell line was established with TAP2 overexpression. The effects of elevated TAP2 expression on GBM cell function was evaluated using various assays, including the Transwell migration, scratch, and clonal formation assays.

Results: TAP2 exhibited aberrantly expression in tumor tissues with genomic alterations. TAP2 significantly correlates with poor prognosis across various cancers. It was also involved in immune-related pathways, immune infiltration, and immune checkpoint regulation, thereby influencing the tumor microenvironment and immune response to cancer. TAP2 was identified as a potential predictor of immunotherapy response and screened for potential targeted inhibitors for future therapeutic interventions.

Conclusions: Our findings suggest that TAP2 may serve as a promising prognostic marker and immune target in human cancers, warranting further investigation into its role in tumor immunity.