CCNE2 promotes cisplatin resistance and affects prognosis of head and neck squamous cell carcinoma by targeting MNAT1.

Cell cycle protein E2 (CCNE2) is a member of the Cyclin family, known for driving tumor cell proliferation and invasion. However, the mechanism of its action in head and neck squamous cell carcinoma (HNSCC) remains unclear. The aim of this study is to investigate the relationship between CCNE2 and cisplatin resistance and survival prognosis of head and neck squamous cell carcinoma. We performed transcriptomic sequencing of HNSCC and HNSCC/DDP. Kaplan-Meier analysis and COX regression analysis were used to evaluate the relationship between CCNE2 expression and survival prognosis of HNSCC patients. Multiple potential biological functions of CCNE2 in HNSCC were identified using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). Single-sample gene set enrichment analysis (ssGSEA) was used to explore tumor immune infiltration. The potential mechanism of CCNE2 was explored by molecular docking and immunoprecipitation. Cell migration, cell invasion and cell proliferation assays were used to investigate the mechanism of CCNE2 in HNSCC. CCNE2 is up-regulated in HNSCC tissues and cell lines and is associated with poor prognosis. The high expression of CCNE2 in HNSCC is associated with clinical significance. GO and KEGG analysis showed that ccne2 related genes may be involved in the regulation of DNA double-strand break repair and DNA metabolic process. CCNE2 expression was positively correlated with the infiltration levels of helper T cells, Tcm cells and Th2 cells, and negatively correlated with the infiltration levels of DC, neutrophils and pDC. CCNE2 regulates the invasion, migration and proliferation of HNSCC cells by targeting MNAT1. CCNE2 also altered cisplatin resistance in HNSCC/DDP. CCNE2 may be an independent prognostic biomarker of HNSCC through MNAT1, which provides new ideas for cisplatin resistance and therapeutic targets of HNSCC.