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Current therapies for pancreatic ductal cancer ( PDAC ) do not sufficiently control distant metastasis. Thus, new therapeutic targets are urgently needed. Numerous studies have suggested that the epithelial‐mesenchymal transition ( EMT ) is pivotal for metastasis of carcinomas. The fact that the  EMT  is reversible suggests the possibility that it is induced by an epigenetic mechanism. In this study, we aimed to investigate the role of histone deacetylase 1 ( HDAC 1), which is an epigenetic mechanism on distant metastasis of  PDAC . We investigated the  HDAC 1 expression in 103 resected  PDAC  specimens obtained from patients who were treated with/without preoperative therapy using immunohistochemistry. To validate the findings in the clinical samples, we evaluated the  HDAC 1 activity, the  EMT ‐associated genes and the migration/invasion ability in vitro, and performed an  HDAC 1 inhibitor assay. The high expression of  HDAC 1 in clinical samples was significantly associated with poor progression‐free survival, especially distant metastasis‐free survival. In vitro,  HDAC 1 inhibitors decreased the invasion ability and reversed the  EMT  change; the only factor to show a concomitant decrease was the expression of  SNAIL . We confirmed that the  HDAC 1 expression was associated with the  SNAIL  expression in clinical samples. Moreover, the resistant cells and parental cells did not show any significant differences in the expression of  HDAC 1; this was consistent with the finding that preoperative therapy did not alter the  HDAC 1 expression in clinical samples. The targeting of  HDAC 1, which could suppress metastasis by inhibiting the  EMT , is a promising treatment option for  PDAC .

Role of histone deacetylase 1 in distant metastasis of pancreatic ductal cancer