ArticleExperimental and therapeutic medicine2018
MGCD0103 induces apoptosis and simultaneously increases the expression of NF-κB and PD-L1 in classical Hodgkin's lymphoma.
Article in Experimental and therapeutic medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- The Epigenetic Architecture of Classical Hodgkin Lymphoma: Lineage Erasure, Immune Escape, and Therapeutic Reprogramming.Medicina (Kaunas, Lithuania) · 2026Review
- Review
- Safety and Efficacy of Tinostamustine in a Subpopulation of Patients With Relapsed/Refractory Hodgkin Lymphoma From a Phase I Trial.Hematological oncology · 2025Article
- PD-L1 Expression in Neoplastic and Immune Cells of Thymic Epithelial Tumors: Correlations with Disease Characteristics and HDAC Expression.Biomedicines · 2024Article
- Article
- Repurposable Drugs for Immunotherapy and Strategies to Find Candidate Drugs.Pharmaceutics · 2023Review
- Epigenetic modifications: Critical participants of the PD‑L1 regulatory mechanism in solid tumors (Review).International journal of oncology · 2022Review
- HDAC inhibitors overcome immunotherapy resistance in B-cell lymphoma.Protein & cell · 2020Review
- Role of HDACs in normal and malignant hematopoiesis.Molecular cancer · 2020Review
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
At present there is no consensus on the treatment of classical Hodgkin's lymphoma (CHL) following relapse. The aim of the present study was to access the class I-selective histone deacetylase (HDAC) inhibitor (HDACI) MGCD0103 on the expression levels of Bcl-2, nuclear factor (NF)-κB and programmed death-ligand 1 (PD-L1) in CHL, to explore the possible therapeutic value of MGCD0103 in combined relative target drugs for patients with CHL. In L1236 and L428 cell lines, apoptosis and cell cycle stage were identified using flow cytometry, and the effects of HDACI on CHL were assessed in terms of Bcl-2, NF-κB and PD-L1 expression levels, which were detected by western blotting and co-focusing experiments. The results demonstrated that MGCD0103 could induce cell apoptosis and cell cycle arrest, down-regulate Bcl-2 and increase NF-κB and PD-L1 expression levels in L1236 and L428 cell lines. MGCD0103 decreases Bcl-2 levels and upregulates PD-L1, which indicates that the combined use of HDACIs and a PD-L1 inhibitor in theory may improve treatment outcomes in patients with CHL. MGCD0103 may also up-regulate NF-κB, which seems to induce resistance towards anti-apoptotic drugs. Clinical trials combining HDACIs with NF-κB and/or PD-L1 inhibitors should be designed to further improve treatment outcomes for patients with CHL.
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