Zinc finger protein 514 promotes esophageal cancer progression by enhancing cell proliferation, migration and invasion.

Esophageal cancer (EC), a malignant tumor occurring in the upper gastrointestinal tract, is the seventh most common cancer worldwide. Zinc finger proteins (ZNFs), the most abundant family of transcription factors in humans, serve an important role in the initiation and progression of various malignant tumors. However, the function of ZNFs in EC remains unclear. The present study aimed to elucidate the role of ZNF514 in the development and progression of EC and to investigate its underlying mechanism. The mRNA and protein expression levels of ZNF514 were assessed using reverse transcription‑quantitative PCR and western blotting. To assess functional roles, multiple cellular assays were performed, including 5‑ethynyl‑2'‑deoxyuridine incorporation, Cell Counting Kit‑8, wound healing, colony formation and Transwell assays. Subsequently, for transcriptomics analysis, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses, Gene Set Enrichment Analysis and Ingenuity Pathway Analysis (IPA) were performed. In EC, ZNF514 exhibited high expression at both the mRNA and protein levels. Additionally, ZNF514 influenced the migration, invasion and proliferation of EC cells. Gene enrichment analyses and IPA demonstrated that ZNF514 knockdown significantly affected multiple signaling pathways, such as Fcγ receptors, the complement system, G‑protein coupled receptors (GPCRs)‑related receptors, the ribosomal S6 kinase (RSK) pathway, Ras/MEK, PI3K/AKT, STAT3, nucleotide‑binding oligomerization domain‑containing protein (NOD) and NF‑κB pathways. In conclusion, the present study indicated that the anticancer mechanisms induced by ZNF514 knockdown may be related to the enhancement of Fcγ receptor and complement system activation, as well as the inhibition of GPCR, RSK, Ras/MEK, PI3K/AKT, STAT3, NOD1/2 and NF‑κB pathways.