ArticleCancer science2018
Role of histone deacetylase 1 in distant metastasis of pancreatic ductal cancer.
Article in Cancer science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed.
- Review
- IL-33 released during liver resection facilitates intrahepatic cholangiocarcinoma growth via cytokine secretion in cancer-associated fibroblasts.British journal of cancer · 2026Article
- Tumor Endothelial Cells Induce M2 Macrophage Polarization via IL-4, Enhancing Tumor Growth in Hepatocellular Carcinoma.Cancer science · 2025Article
- Twist1 Regulates the Immune Checkpoint VISTA and Promotes the Proliferation, Migration and Progression of Pancreatic Cancer Cells.Journal of cellular and molecular medicine · 2025Article
- Establishment of a nomogram model for predicting distant metastasis in pancreatic ductal adenocarcinoma: a comparative analysis of different lymph node staging systems based on the SEER database.Scientific reports · 2024Article
- Article
- KLK10 derived from tumor endothelial cells accelerates colon cancer cell proliferation and hematogenous liver metastasis formation.Cancer science · 2024Article
- MicroRNA-26a-5p is a reliable biomarker in the adjuvant setting for pancreatic ductal adenocarcinoma.PloS one · 2024Article
- Epigenetic control of pancreatic cancer metastasis.Cancer metastasis reviews · 2023Review
- Targeting histone deacetylases for cancer therapy: Trends and challenges.Acta pharmaceutica Sinica. B · 2023Review
- Rubicon can predict prognosis in patients with pancreatic ductal adenocarcinoma after neoadjuvant chemoradiotherapy.International journal of clinical oncology · 2023Article
- Histone Modifications Represent a Key Epigenetic Feature of Epithelial-to-Mesenchyme Transition in Pancreatic Cancer.International journal of molecular sciences · 2023Review
- Differential molecular mechanistic behavior of HDACs in cancer progression.Medical oncology (Northwood, London, England) · 2022Review
- Inhibition of Clusterin Represses Proliferation by Inducing Cellular Senescence in Pancreatic Cancer.Annals of surgical oncology · 2022Article
- Targeting pancreatic cancer immune evasion by inhibiting histone deacetylases.World journal of gastroenterology · 2022Review
- Targeting Histone Deacetylases in Idiopathic Pulmonary Fibrosis: A Future Therapeutic Option.Cells · 2022Review
- Tumor endothelial cell-induced CD8Cancer science · 2022Article
- The histone deacetylase inhibitor M344 as a multifaceted therapy for pancreatic cancer.PloS one · 2022Article
- Clinical Utility of Epigenetic Changes in Pancreatic Adenocarcinoma.Epigenomes · 2021Review
- Serum exosomal miR-638 is a prognostic marker of HCC via downregulation of VE-cadherin and ZO-1 of endothelial cells.Cancer science · 2021Observational
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 (HDAC1), which is an epigenetic mechanism on distant metastasis of PDAC. We investigated the HDAC1 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 HDAC1 activity, the EMT-associated genes and the migration/invasion ability in vitro, and performed an HDAC1 inhibitor assay. The high expression of HDAC1 in clinical samples was significantly associated with poor progression-free survival, especially distant metastasis-free survival. In vitro, HDAC1 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 HDAC1 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 HDAC1; this was consistent with the finding that preoperative therapy did not alter the HDAC1 expression in clinical samples. The targeting of HDAC1, which could suppress metastasis by inhibiting the EMT, is a promising treatment option for PDAC.
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