ArticleJournal of immunology (Baltimore, Md. : 1950)2015
Bortezomib inhibits expression of TGF-β1, IL-10, and CXCR4, resulting in decreased survival and migration of cutaneous T cell lymphoma cells.
Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 47 citations in OpenAlex.
- Assessing the Efficacy of Bortezomib and Dexamethasone for Induction and Maintenance Therapy in Relapsed/Refractory Cutaneous T-Cell Lymphoma: A Phase II CISL1701/BIC Study.Cancer research and treatment · 2025Trial
- Trial
- Migration and invasion inhibitory protein inhibits M2 macrophage polarization to suppress colorectal cancer progression through the STING-NFκB2-IL10 axis.Cancer biology & medicine · 2026Article
- Chemokine Networks in Cutaneous T Cell Lymphoma: Tumor Microenvironment Remodeling and Therapeutic Targets.Current issues in molecular biology · 2026Review
- Interplay of oxidative stress and antioxidant mechanisms in cancer development and progression.Archives of toxicology · 2026Review
- Review
- Review
- Chemo-free salvage treatment outperforms traditional chemotherapy in advanced lines of relapsed/refractory subcutaneous panniculitis-like T-cell lymphoma.Frontiers in immunology · 2024Article
- Mechanisms underlying reversed TRAIL sensitivity in acquired bortezomib-resistant non-small cell lung cancer cells.Cancer drug resistance (Alhambra, Calif.) · 2024Article
- New Molecular and Biological Markers in Cutaneous T Cell Lymphoma: Therapeutic Implications.Current hematologic malignancy reports · 2023Review
- Skin infiltrating NK cells in cutaneous T-cell lymphoma are increased in number and display phenotypic alterations partially driven by the tumor.Frontiers in immunology · 2023Article
- Mitochondrial oxidative stress in the tumor microenvironment and cancer immunoescape: foe or friend?Journal of biomedical science · 2022Review
- Article
- A novel lncRNA TCLlnc1 promotes peripheral T cell lymphoma progression through acting as a modular scaffold of HNRNPD and YBX1 complexes.Cell death & disease · 2021Article
- The changing therapeutic landscape, burden of disease, and unmet needs in patients with cutaneous T-cell lymphoma.British journal of haematology · 2021Review
- Connectivity map-based drug repositioning of bortezomib to reverse the metastatic effect of GALNT14 in lung cancer.Oncogene · 2020Article
- Suppressors of Cytokine Signaling (SOCS)1 and SOCS3 Proteins Are Mediators of Interleukin-10 Modulation of Inflammatory Responses Induced byMediators of inflammation · 2020Article
- Analysis of endogenous and exogenous tumor upregulated promoter expression in canine tumors.PloS one · 2020Article
- Racial Differences in Immunological Landscape Modifiers Contributing to Disparity in Prostate Cancer.Cancers · 2019Review
- [Association of interleukin-10 gene polymorphism with enterovirus 71 infection in children].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2019Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Increased expression of the immunosuppressive cytokines, TGF-β1 and IL-10, is a hallmark of the advanced stages of cutaneous T cell lymphoma (CTCL), where it has been associated with suppressed immunity, increased susceptibility to infections, and diminished antitumor responses. Yet, little is known about the transcriptional regulation of TGF-β1 and IL-10 in CTCL, and about their function in regulating the CTCL cell responses. In this article, we show that TGF-β1 and IL-10 expression in CTCL cells is regulated by NF-κB and suppressed by bortezomib (BZ), which has shown promising results in the treatment of CTCL. However, although the TGF-β1 expression is IκBα dependent and is regulated by the canonical pathway, the IL-10 expression is IκBα independent, and its inhibition by BZ is associated with increased promoter recruitment of p52 that characterizes the noncanonical pathway. TGF-β1 suppression decreases CTCL cell viability and increases apoptosis, and adding exogenous TGF-β1 increases viability of BZ-treated CTCL cells, indicating TGF-β1 prosurvival function in CTCL cells. In addition, TGF-β1 suppression increases expression of the proinflammatory cytokines IL-8 and IL-17 in CTCL cells, suggesting that TGF-β1 also regulates the IL-8 and IL-17 expression. Importantly, our results demonstrate that BZ inhibits expression of the chemokine receptor CXCR4 in CTCL cells, resulting in their decreased migration, and that the CTCL cell migration is mediated by TGF-β1. These findings provide the first insights into the BZ-regulated TGF-β1 and IL-10 expression in CTCL cells, and indicate that TGF-β1 has a key role in regulating CTCL survival, inflammatory gene expression, and migration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.