ArticleBlood2017
Bifurcated BACH2 control coordinates mantle cell lymphoma survival and dispersal during hypoxia.
Article in Blood, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- CD40LG/CD28-Mediated Rho GTPase Signaling Drives Survival and Chemoresistance in Non-ETP T-ALL.International journal of molecular sciences · 2026Article
- Hypoxia-induced cysteine metabolism reprogramming is crucial for the tumorigenesis of colorectal cancer.Redox biology · 2024Article
- BACH2-mediated CD28 and CD40LG axes contribute to pathogenesis and progression of T-cell lymphoblastic leukemia.Cell death & disease · 2024Article
- [Expression and significance of jumonji domain-containing protein 2B and hypoxia inducible factor-1α in non-Hodgkin lymphoma tissues in children].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2023Article
- Targeting the tumor microenvironment in B-cell lymphoma: challenges and opportunities.Journal of hematology & oncology · 2021Review
- 3-Methyladenine but not antioxidants to overcome BACH2-mediated bortezomib resistance in mantle cell lymphoma.Cancer cell international · 2021Article
- BACH2-mediated FOS confers cytarabine resistance via stromal microenvironment alterations in pediatric ALL.Cancer science · 2021Observational
- Article
- Genomic profiles and clinical outcomes of de novo blastoid/pleomorphic MCL are distinct from those of transformed MCL.Blood advances · 2020Article
- Influence of Casein kinase II inhibitor CX-4945 on BCL6-mediated apoptotic signaling in B-ALL in vitro and in vivo.BMC cancer · 2020Article
- Review
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5 authors at 3 institutions in 1 country.
Funding
Abstract
BACH2, a B-cell-specific transcription factor, plays a critical role in oxidative stress-mediated drug resistance in mantle cell lymphoma (MCL); however, the biological functions of BACH2 and its regulation of B-cell malignancies in chronic hypoxic microenvironment have not been studied. Here, we found that silencing BACH2 led to not only increased tumor formation and colony formation but also increased tumor dispersal to spleen and bone marrow. Decreased BACH2 levels in patients were also correlated with bone marrow and gastrointestinal dispersal of MCL and blastoid subtypes of MCL. Unexpectedly, decreased BACH2 levels in dispersed MCL cells were due to direct transcriptional repression by hypoxia-induced factor 1α (HIF-1α) and increased heme-mediated protein degradation. In normoxic conditions, BACH2 was able to modulate HIF-1α degradation by suppressing prolyl hydroxylase 3 expression. Bifurcated BACH2 controls during hypoxia and normoxia coordinate not only MCL tumor dispersal but also drug resistance, including bortezomib resistance, via plasmacytic differentiation. Our data highlight an interactive relationship between tumor cells and local microenvironment and the mechanisms of B-cell transcription factor in the regulation of MCL dispersal.
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