ArticleInternational journal of molecular sciences2018
Pharmacological Inhibition of Class IIA HDACs by LMK-235 in Pancreatic Neuroendocrine Tumor Cells.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Epigenetic Dysregulation of Somatostatin Receptors (SSTR) 1-5 and Therapeutic Implications in Neuroendocrine and Non-Neuroendocrine Malignancies.International journal of cancer · 2026Review
- Are HDAC and Glutamine Synthetase Expression Levels Associated with Ga68-DOTATATE PET/CT Data and Prognosis in Gastroenteropancreatic Neuroendocrine Tumours?Medicina (Kaunas, Lithuania) · 2025Article
- Dendritic cells: understanding ontogeny, subsets, functions, and their clinical applications.Molecular biomedicine · 2025Review
- Development of Glutathione Hydrogel Carriers Containing Zinc Oxide Microparticles for Skin Regeneration Processes.International journal of molecular sciences · 2025Article
- Design and radiosynthesis of class-IIa HDAC inhibitor with high molar activity via repositioning theScientific reports · 2024Article
- Pancreatic Neuroendocrine Tumors: Signaling Pathways and Epigenetic Regulation.International journal of molecular sciences · 2024Review
- Epigenetic drugs in somatostatin type 2 receptor radionuclide theranostics and radiation transcriptomics in mouse pheochromocytoma models.Theranostics · 2023Article
- Epigenetic regulation of SSTFrontiers in endocrinology · 2023Article
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- A Selective Histone Deacetylase Inhibitor Induces Autophagy and Cell Death via SCNN1A Downregulation in Glioblastoma Cells.Cancers · 2022Article
- Development of a cancer cells self‑activating and miR‑125a‑5p expressing poly‑pharmacological nanodrug for cancer treatment.International journal of molecular medicine · 2022Article
- MARK2 regulates chemotherapeutic responses through class IIa HDAC-YAP axis in pancreatic cancer.Oncogene · 2022Article
- The Effect of VPA Treatment on Radiolabeled DOTATATE Uptake: Differences Observed In Vitro and In Vivo.Pharmaceutics · 2022Article
- Selective Inhibition of Histone Deacetylase Class IIa With MC1568 Ameliorates Podocyte Injury.Frontiers in medicine · 2022Article
- The Critical Role of MMP13 in Regulating Tooth Development and Reactionary Dentinogenesis Repair Through the Wnt Signaling Pathway.Frontiers in cell and developmental biology · 2022Article
- Review
- Potential for Increasing Uptake of RadiolabeledCancer biotherapy & radiopharmaceuticals · 2021Article
- Comparing the Effect of Multiple Histone Deacetylase Inhibitors on SSTR2 Expression and [Cancers · 2021Article
- Theranostics in neuroendocrine tumors: an overview of current approaches and future challenges.Reviews in endocrine & metabolic disorders · 2021Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histone deacetylases (HDACs) play a key role in epigenetic mechanisms in health and disease and their dysfunction is implied in several cancer entities. Analysis of expression patterns in pancreatic neuroendocrine tumors (pNETs) indicated HDAC5 to be a potential target for future therapies. As a first step towards a possible treatment, the aim of this study was to evaluate the in vitro cellular and molecular effects of HDAC5 inhibition in pNET cells. Two pNET cell lines, BON-1 and QGP-1, were incubated with different concentrations of the selective class IIA HDAC inhibitor, LMK-235. Effects on cell viability were determined using the resazurin-assay, the caspase-assay, and Annexin-V staining. Western Blot and immunofluorescence microscopy were performed to assess the effects on HDAC5 functionality. LMK-235 lowered overall cell viability by inducing apoptosis in a dose- and time-dependent manner. Furthermore, acetylation of histone-H3 increased with higher LMK-235 concentrations, indicating functional inhibition of HDAC4/5. Immunocytochemical analysis showed that proliferative activity (phosphohistone H3 and Ki-67) decreased at highest concentrations of LMK-235 while chromogranin and somatostatin receptor 2 (SSTR2) expression increased in a dose-dependent manner. HDAC5 expression was found to be largely unaffected by LMK-235. These findings indicate LMK-235 to be a potential therapeutic approach for the development of an effective and selective pNET treatment.
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