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Published on: June 16, 2019
Depsipeptide induces cell death in Hodgkin lymphoma-derived cell lines
Ingo Hartlapp1, Christian Pallasch, Ganna Weibert
1Department of Internal Medicine II, University Hospital of Wuerzburg, 97080 Wuerzburg, Germany.
Abstract:
A variety of genetic and epigenetic abnormalities were characterized over the last years in Hodgkin and Reed-Sternberg (H-RS) cells of classic Hodgkin Lymphoma (cHL). It was speculated that simultaneous inhibition of multiple signalling pathways might be a promising strategy to target this tumor entity. In the present study we tested the effect of histone deacetylase (HDAC) inhibition using depsipeptide (also known as romidepsin, FK228, FR901228 or NSC-630176) in cHL cell lines in vitro. Molecular mechanisms of toxicity were analyzed using RNA expression analysis and functional assays. It is shown that depsipeptide is effective at submicromolar concentrations and acts mainly by apoptosis induction, upregulation of p21 and cell cycle inhibition in G2/M. Of special note, HDAC mediated toxicity in H-RS cells does not require RelA/p65 downregulation, which was previously shown to drive the malignant phenotype of H-RS cells. In summary, depsipeptide induced protein acetylation results in transcriptional changes of a large number of pathogenetically relevant genes and increased RelA/p65 binding activity in cHL cell lines. Our preclinical data suggest that HDAC inhibition using depsipeptide might be a promising approach for the treatment of cHL patients.
Insights
Histone deacetylase (HDAC) inhibition using depsipeptide effectively targets classic Hodgkin Lymphoma (cHL) cell lines. This approach induces apoptosis and inhibits cell cycle progression, suggesting potential for cHL patient treatment.
Area of Science:
- Oncology
- Molecular Biology
- Epigenetics
Background:
- Classic Hodgkin Lymphoma (cHL) is characterized by genetic and epigenetic abnormalities in Hodgkin and Reed-Sternberg (H-RS) cells.
- Simultaneous inhibition of multiple signaling pathways is a potential therapeutic strategy for cHL.
Purpose of the Study:
- To investigate the efficacy of histone deacetylase (HDAC) inhibition using depsipeptide in cHL cell lines.
- To elucidate the molecular mechanisms underlying depsipeptide's anti-cancer effects in cHL.
Main Methods:
- In vitro study using cHL cell lines treated with depsipeptide.
- Analysis of molecular mechanisms via RNA expression analysis and functional assays.
Main Results:
- Depsipetide demonstrated efficacy at submicromolar concentrations, primarily inducing apoptosis and inhibiting cell cycle progression at G2/M.
- HDAC inhibition-mediated toxicity in H-RS cells occurred independently of RelA/p65 downregulation.
- Depsipetide induced protein acetylation, leading to transcriptional changes in pathogenetically relevant genes and increased RelA/p65 binding activity.
Conclusions:
- HDAC inhibition with depsipeptide shows promise as a therapeutic strategy for classic Hodgkin Lymphoma.
- Preclinical data suggest depsipeptide's potential for treating cHL patients.
