BCAP29/31 as a Poor Prognostic Biomarker for Head and Neck Squamous Carcinoma: Impacting the TGFβ1/Smad- EMT Pathway

Abstract Objectives This study aimed to investigate the possible mechanism of action of BCAP29/31 in head and neck squamous cell carcinoma (HNSC) and to provide clues for finding new therapeutic targets for HNSC. Materials and methods We performed several data analyses including Kyoto Encyclopedia of the Genome (KEGG) and Gene Ontology (GO) analyses, immune infiltration, and single-cell analyses using databases such as TIMER2.0, TISIDB, STRING, Metascape, and GRNdb. The possible mechanism of action of BCAP29/31 in HNSC was investigated and validated using Q-PCR real-time fluorescence quantitative analysis. Results BCAP29/31 manifested a trend of overexpression and a certain mutation rate in HNSC. BCAP29/31 are each other's members of the protein interactions network and are associated with calcineurin binding and vesicle transport function. BCAP29/31 demonstrated the same trend correlating with CD8+ T and B cells, and abnormal associations with endothelial cell and macrophage infiltration levels. Conclusion The overexpression of BCAP29/31 is correlated with poor prognosis in HNSC and may affect the TGFβ1/Smad epithelial-mesenchymal transition (EMT) process. Overexpression of BCAP29/31 may be a factor causing the aberrant level of immune infiltration in HNSC. In conjunction with existing clinical treatment options, knockdown of BACP29/31 or targeted elimination of tumor-associated macrophage M2 tumor-associated macrophages (TAM M2) may help improve anti-PD-1/PD-L1 efficacy. Clinical Relevance Our study elucidated the mechanism of action in which BCAP29/31 may be involved in HNSC. The results supported the use of BCAP29/31 as a poor prognostic biomarker for HNSC and offered new insights to improve the efficacy of anti-PD-1/PD-L1 therapies in HNSC in the future.