ArticleCancer drug resistance (Alhambra, Calif.)2021
Expression of histone deacetylase (HDAC) family members in bortezomib-refractory multiple myeloma and modulation by panobinostat.
Article in Cancer drug resistance (Alhambra, Calif.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- HDAC1 has intrinsic protease activity and regulates transcription through clipping histone H3 N-terminal tail.Cell death and differentiation · 2026Article
- Selective molecular inhibition of the HDAC6 ZnF-UBP binding domain impairs multiple myeloma cell function.Cell death discovery · 2025Article
- Therapeutic role of histone deacetylase inhibition in anMolecular medicine reports · 2024Article
- Targeting apoptotic pathways for cancer therapy.The Journal of clinical investigation · 2024Review
- Targeted small molecule therapy and inhibitors for lymphoma.Future medicinal chemistry · 2024Review
- The Status and Prospects of Epigenetics in the Treatment of Lymphoma.Frontiers in oncology · 2022Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
aimMultiple myeloma (MM) is a hematological malignancy of antibody-producing mature B cells or plasma cells. The proteasome inhibitor, bortezomib, was the first-in-class compound to be FDA approved for MM and is frequently utilized in induction therapy. However, bortezomib refractory disease is a major clinical concern, and the efficacy of the pan-histone deacetylase inhibitor (HDACi), panobinostat, in bortezomib refractory disease indicates that HDAC targeting is a viable strategy. Here, we utilized isogenic bortezomib resistant models to profile HDAC expression and define baseline and HDACi-induced expression patterns of individual HDAC family members in sensitive
methodsGene expression of HDAC family members in two sets of isogenic bortezomib sensitive or resistant myeloma cell lines was examined. These cell lines were subsequently treated with HDAC inhibitors: panobinostat or vorinostat, and HDAC expression was evaluated. CRISPR/Cas9 knockdown and pharmacological inhibition of specific HDAC family members were conducted.
resultsInterestingly, HDAC6 and HDAC7 were significantly upregulated and downregulated, respectively, in bortezomib-resistant cells. Panobinostat was effective at inducing cell death in these lines and modulated HDAC expression in cell lines and patient samples. Knockdown of HDAC7 inhibited cell growth while pharmacologically inhibiting HDAC6 augmented cell death by panobinostat.
conclusionOur data revealed heterogeneous expression of individual HDACs in bortezomib sensitive
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