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Clin Epigenetics ; 16(1): 102, 2024 Aug 03.
Article in English | MEDLINE | ID: mdl-39097736

ABSTRACT

BACKGROUND: Oesophageal cancer remains a challenging disease with high mortality rates and few therapeutic options. In view of these difficulties, epigenetic drugs have emerged as potential alternatives for patient care. The goal of this study was to evaluate the effect and biological consequences of Panobinostat treatment, an HDAC (histone deacetylase) inhibitor already approved for treatment of patients with multiple myeloma, in oesophageal cell lines of normal and malignant origin, with the latter being representative of the two main histological subtypes: adenocarcinoma and squamous cell carcinoma. RESULTS: Panobinostat treatment inhibited growth and hindered proliferation, colony formation and invasion of oesophageal cancer cells. Considering HDAC tissue expression, HDAC1 was significantly upregulated in normal oesophageal epithelium in comparison with tumour tissue, whereas HDAC3 was overexpressed in oesophageal cancer compared to non-malignant mucosa. No differences between normal and tumour tissue were observed for HDAC2 and HDAC8 expression. CONCLUSIONS: Panobinostat exposure effectively impaired malignant features of oesophageal cancer cells. Because HDAC3 was shown to be overexpressed in oesophageal tumour samples, this epigenetic drug may represent an alternative therapeutic option for oesophageal cancer patients.


Subject(s)
Adenocarcinoma , Carcinoma, Squamous Cell , Cell Proliferation , Esophageal Neoplasms , Histone Deacetylase Inhibitors , Histone Deacetylases , Panobinostat , Humans , Panobinostat/pharmacology , Panobinostat/therapeutic use , Panobinostat/administration & dosage , Esophageal Neoplasms/drug therapy , Esophageal Neoplasms/genetics , Esophageal Neoplasms/pathology , Cell Line, Tumor , Adenocarcinoma/drug therapy , Adenocarcinoma/genetics , Adenocarcinoma/pathology , Histone Deacetylases/genetics , Histone Deacetylases/metabolism , Cell Proliferation/drug effects , Carcinoma, Squamous Cell/drug therapy , Carcinoma, Squamous Cell/genetics , Histone Deacetylase Inhibitors/pharmacology , Histone Deacetylase Inhibitors/therapeutic use , Histone Deacetylase 1/genetics , Histone Deacetylase 2/genetics , Repressor Proteins/genetics , Hydroxamic Acids/pharmacology , Hydroxamic Acids/therapeutic use , Epigenesis, Genetic/drug effects , Gene Expression Regulation, Neoplastic/drug effects , Antineoplastic Agents/pharmacology , Antineoplastic Agents/therapeutic use , Indoles/pharmacology , Indoles/therapeutic use , Esophageal Squamous Cell Carcinoma/drug therapy , Esophageal Squamous Cell Carcinoma/genetics , Esophageal Squamous Cell Carcinoma/pathology
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