ArticleMolecular cancer research : MCR2011
Bortezomib induces nuclear translocation of IκBα resulting in gene-specific suppression of NF-κB--dependent transcription and induction of apoptosis in CTCL.
Article in Molecular cancer research : MCR, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 96 citations in OpenAlex.
- Bortezomib is significantly beneficial for de novo pediatric AML patients with low phosphorylation of the NF-κB subunit RelA.Proteomics. Clinical applications · 2022Trial
- CRISPR-Cas9 screen reveals that inhibition of enhancer of zeste homolog 2 sensitizes malignant T cells to dimethyl-fumarate-induced cell death.The FEBS journal · 2026Article
- Decoding NF-κB: nucleocytoplasmic shuttling dynamics, synthetic modulation and post-therapeutic behavior in cancer.Molecular biology reports · 2025Review
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- Transcriptomic and proteomic analysis of tumor suppressive effects of GZ17-6.02 against mycosis fungoides.Scientific reports · 2024Article
- PBRM1 loss redirects chromatin remodelling complex to recruit oncogenic factors.Nature cell biology · 2023Article
- PBRM1-deficient PBAF complexes target aberrant genomic loci to activate the NF-κB pathway in clear cell renal cell carcinoma.Nature cell biology · 2023Article
- Review
- PEG10 amplification at 7q21.3 potentiates large-cell transformation in cutaneous T-cell lymphoma.Blood · 2022Article
- Dual-Targeted Therapy Circumvents Non-Genetic Drug Resistance to Targeted Therapy.Frontiers in oncology · 2022Review
- Bortezomib suppresses self-renewal and leukemogenesis of leukemia stem cell by NF-ĸB-dependent inhibition of CDK6 in MLL-rearranged myeloid leukemia.Journal of cellular and molecular medicine · 2021Article
- AeMOPE-1, a Novel Salivary Peptide FromFrontiers in immunology · 2021Article
- Antineoplastic effect of a novel nanosized curcumin on cutaneous T cell lymphoma.Oncology letters · 2020Article
- Non-covalent immunoproteasome inhibitors induce cell cycle arrest in multiple myeloma MM.1R cells.Journal of enzyme inhibition and medicinal chemistry · 2019Article
- The IAP antagonist birinapant potentiates bortezomib anti-myeloma activity in vitro and in vivo.Journal of hematology & oncology · 2019Article
- Induction of autophagy-dependent apoptosis in cancer cells through activation of ER stress: an uncovered anti-cancer mechanism by anti-alcoholism drug disulfiram.American journal of cancer research · 2019Article
- Novel insights and therapeutic approaches in idiopathic multicentric Castleman disease.Hematology. American Society of Hematology. Education Program · 2018Review
- Review
- The proto-oncogene Bcl3 induces immune checkpoint PD-L1 expression, mediating proliferation of ovarian cancer cells.The Journal of biological chemistry · 2018Article
- Chemical modulation of transcription factors.MedChemComm · 2018Review
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Cutaneous T-cell lymphoma (CTCL) is characterized by constitutive activation of nuclear factor κB (NF-κB), which plays a crucial role in the survival of CTCL cells and their resistance to apoptosis. NF-κB activity in CTCL is inhibited by the proteasome inhibitor bortezomib; however, the mechanisms remained unknown. In this study, we investigated mechanisms by which bortezomib suppresses NF-κB activity in CTCL Hut-78 cells. We demonstrate that bortezomib and MG132 suppress NF-κB activity in Hut-78 cells by a novel mechanism that consists of inducing nuclear translocation and accumulation of IκBα (nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha), which then associates with NF-κB p65 and p50 in the nucleus and inhibits NF-κB DNA binding activity. Surprisingly, however, while expression of NF-κB-dependent antiapoptotic genes cIAP1 and cIAP2 is inhibited by bortezomib, expression of Bcl-2 is not suppressed. Chromatin immunoprecipitation indicated that cIAP1 and cIAP2 promoters are occupied by NF-κB p65/50 heterodimers, whereas Bcl-2 promoter is occupied predominantly by p50/50 homodimers. Collectively, our data reveal a novel mechanism of bortezomib function in CTCL and suggest that the inhibition of NF-κB-dependent gene expression by bortezomib is gene specific and depends on the subunit composition of NF-κB dimers recruited to NF-κB-responsive promoters.
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