This study aimed to investigate the functions of and in esophageal cancer (EC). Bioinformatics analysis, qRT-PCR and western blot were used to analyze the expression levels. Biological functions were evaluated using cell-counting kit 8, colony formation, Transwell assays and flow cytometry. FISH was used to detect subcellular localization, and methylation-specific PCR determined gene methylation levels. Animal experiments validated the impact on tumor progression. and were highly methylated and downregulated in EC. Overexpression of up-regulated the expression of , thereby inhibiting EC cell viability and metastasis, promoting apoptosis and inhibiting tumor growth. Low expression of / mediated by DNA hypermethylation facilitates the malignant progression of EC.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11318746PMC
http://dx.doi.org/10.1080/17501911.2024.2342229DOI Listing

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