Loss of zinc-finger protein 331 (ZNF331) expression was reported in gastric cancer. To explore
the regulation of expression and the function of ZNF331 in human esophageal cancer, 11 esophageal
cancer cell lines, 7 cases of normal esophageal mucosa and 99 cases of primary esophageal
squamous cancer were employed. Methylation specific PCR, semi-quantitive reverse transcriptase PCR, immunohistochemistry,
western blot, flow cytometry, wound healing and transwell assay were used. The expression of ZNF331 was silenced
by promoter region hypermethylation in 8 of 11 esophageal cancer cell lines. 56.5% (56/99) of primary human
esophageal cancer was methylated, but no methylation was found in 7 cases of normal esophageal mucosa. The expression
of ZNF331 was reduced in human primary esophageal cancer and reduced expression was associated with promoter
region methylation. No significant change was found in cell viability (P>0.05) and cell phase distribution (P>0.05) before
and after re-expression in KYSE150 and KYSE410 cells. The migration was suppressed by ZNF331 apparently under
wound healing experiment. Re-expression of ZNF331 expression significantly suppressed cell migration and invasion
(P<0.05). In conclusion, ZNF331 is frequently methylated in human esophageal cancer. The expression of ZNF331 is
regulated by promoter region methylation. ZNF331 may suppress esophageal cancer metastasis.
Keywords: Human esophageal cancer, invasion, metastasis, methylation, migration, zinc-finger protein 331.
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