ESCO2 promotes hypopharyngeal carcinoma progression in a STAT1-dependent manner

Abstract

Abstract Background: The establishment of sister chromatid cohesion N-acetyltransferase 2 (ESCO2) is involved in the development of multiple malignancies. However, its role in hypopharyngeal carcinoma (HPC) progression remains uncharacterized. Methods: This study employed bioinformatics to determine the ESCO2 expression in head and neck squamous cell carcinoma (HNSC) and normal tissues. In vitro cell proliferation, migration, apoptosis, and/or cell cycle distribution assays were used to determine the function of ESCO2 and its relationship with STAT1. Xenograft models were established in nude mice to determine ESCO2 in HPC growth in vivo. Coimmunoprecipitation/mass spectrometry (Co-IP/MS) was conducted to identify the potential ESCO2 binding partners. Results: We found that ESCO2 expression was elevated in HNSC tissues, and ESCO2 depletion suppressed tumor cell migration in vitro and inhibited tumor growth in vitro and in vivo. Co-IP/MS and immunoblotting assays revealed the interaction between ESCO2 and STAT1 in HPC cells. ESCO2-mediated suppressive effects on HPC cell proliferation, viability, and migration were compromised by STAT1-overexpression. Conclusions: These findings suggest that ESCO2 is crucial in promoting HPC malignant progression through the STAT1 pathway, and provide novel therapeutic targets for HPC treatment.