ArticlePloS one2013
Nuclear translocation of B-cell-specific transcription factor, BACH2, modulates ROS mediated cytotoxic responses in mantle cell lymphoma.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
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- Comparative Codon Usage Bias of CD2AP and BACH2 Across 49 Vertebrates: Implications for Porcine Macrophage Immunity inBiology · 2026Article
- Therapeutic restoration of miR-96 prevents hearing loss in mice through modulation of noise-induced and genetic pathways.iScience · 2025Article
- The redox sensor KEAP1 facilitates adaptation of T cells to chronic antigen stimulation by preventing hyperactivation.Science immunology · 2024Article
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- SOX11/PRDX2 axis modulates redox homeostasis and chemoresistance in aggressive mantle cell lymphoma.Scientific reports · 2024Article
- Regulation and therapy: the role of ferroptosis in DLBCL.Frontiers in pharmacology · 2024Review
- Oxidative Stress and Inflammation in B-Cell Lymphomas.Antioxidants (Basel, Switzerland) · 2023Review
- 3-Methyladenine but not antioxidants to overcome BACH2-mediated bortezomib resistance in mantle cell lymphoma.Cancer cell international · 2021Article
- Expression of Keap1 and Nrf2 in diffuse large B-cell lymphoma and its clinical significance.Experimental and therapeutic medicine · 2018Article
- The Role of BACH2 in T Cells in Experimental Malaria Caused byFrontiers in immunology · 2018Article
- Targeting Oxidatively Induced DNA Damage Response in Cancer: Opportunities for Novel Cancer Therapies.Oxidative medicine and cellular longevity · 2018Review
- More than Just an Immunosuppressant: The Emerging Role of FTY720 as a Novel Inducer of ROS and Apoptosis.Oxidative medicine and cellular longevity · 2018Review
- ROS-modulated therapeutic approaches in cancer treatment.Journal of cancer research and clinical oncology · 2017Review
- Bifurcated BACH2 control coordinates mantle cell lymphoma survival and dispersal during hypoxia.Blood · 2017Article
- Frequent downregulation of BTB and CNC homology 2 expression in Epstein-Barr virus-positive diffuse large B-cell lymphoma.Cancer science · 2017Article
- microRNA-142 is upregulated by tumor necrosis factor-alpha and triggers apoptosis in human gingival epithelial cells by repressing BACH2 expression.American journal of translational research · 2017Article
- Increase of T and B cells and altered BACH2 expression patterns in bone marrow trephines of imatinib-treated patients with chronic myelogenous leukaemia.Oncology letters · 2016Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACH2, a B-cell specific transcription factor, plays a critical role in oxidative stress-mediated apoptosis. Bortezomib (Velcade(TM)) is widely used to treat relapsed mantle cell lymphoma (MCL) patients despite varying clinical outcomes. As one of the potential mechanisms of action, bortezomib was reported to elicit endoplasmic reticulum (ER) stress which triggers reactive oxygen species (ROS). In the present study, we investigated the redox-sensitive intracellular mechanism that might play a critical role in bortezomib response in MCL cells. We demonstrated that in MCL cells that are sensitive to bortezomib treatments, BACH2 was translocated to the nucleus in response to bortezomib and induced apoptotic responses through the modulation of anti-oxidative and anti-apoptotic genes. On the other hand, in bortezomib resistant cells, BACH2 expression was confined in the cytoplasm and no suppression of antiapoptotic or antioxidative genes, Nrf2, Gss, CAT, HO-1 and MCL1, was detected. Importantly, levels of BACH2 were significantly higher in bortezomib sensitive MCL patient cells, indicating that BACH2 levels could be an indicator for clinical bortezomib responses. BACH2 translocation to the cytoplasm after phosphorylation was inhibited by PI3K inhibitors and combinatory regimens of bortezomib and PI3K inhibitors sensitized MCL cells to bortezomib. These data suggest that cellular distribution of BACH2 in response to ROS determines the threshold for the induction of apoptosis. Therapies that inhibit BACH2 phosphorylation could be the key for increasing bortezomib cytotoxic response in patients.
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