ArticleScientific reports2016
BACH1 Promotes Temozolomide Resistance in Glioblastoma through Antagonizing the Function of p53.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.
- Glioblastoma multiforme (GBM): An overview of current therapies and mechanisms of resistance.Pharmacological research · 2021Pooled it
- Unraveling the role of specificity protein 1 in gliomas: pathophysiology and clinical implications.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Targeting BACH1 by HPPE inhibits the Wnt/β-catenin pathway and malignant phenotype in glioblastoma cells.Apoptosis : an international journal on programmed cell death · 2025Article
- Cryo-mtscATAC-seq for single-cell mitochondrial DNA genotyping and clonal tracing in archived human tissues.bioRxiv : the preprint server for biology · 2025Article
- The Role of the Dysregulation of circRNAs Expression in Glioblastoma Multiforme.Journal of molecular neuroscience : MN · 2025Review
- Single-cell multi-omics sequencing uncovers region-specific plasticity of glioblastoma for complementary therapeutic targeting.Science advances · 2024Article
- Circ_0005015 upregulates BACH1 to promote aggressive behaviors in glioblastoma by sponging microRNA-382-5p.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Transcription factor BACH1 in cancer: roles, mechanisms, and prospects for targeted therapy.Biomarker research · 2024Review
- Advances in Glioblastoma Therapy: An Update on Current Approaches.Brain sciences · 2023Review
- Gene signatures associated with prognosis and chemotherapy resistance in glioblastoma treated with temozolomide.Frontiers in genetics · 2023Article
- Unraveling unique and common cell type-specific mechanisms in glioblastoma multiforme.Computational and structural biotechnology journal · 2022Article
- BTB and CNC homology 1 (Bach1) induces lung cancer stem cell phenotypes by stimulating CD44 expression.Respiratory research · 2021Article
- Identification of glioblastoma immune subtypes and immune landscape based on a large cohort.Hereditas · 2021Article
- High-resolution melting effectively pre-screens for TP53 mutations before direct sequencing in patients with diffuse glioma.Human cell · 2021Article
- Considering the Experimental use of Temozolomide in Glioblastoma Research.Biomedicines · 2020Review
- Combined elevation of TRIB2 and MAP3K1 indicates poor prognosis and chemoresistance to temozolomide in glioblastoma.CNS neuroscience & therapeutics · 2020Article
- Nuclear factor erythroid 2-related factors 1 and 2 are able to define the worst prognosis group among high-risk diffuse large B cell lymphomas treated with R-CHOEP.Journal of clinical pathology · 2019Article
- Fstl1/DIP2A/MGMT signaling pathway plays important roles in temozolomide resistance in glioblastoma.Oncogene · 2019Article
- Deubiquitinating enzyme 4 facilitates chemoresistance in glioblastoma by inhibiting P53 activity.Oncology letters · 2019Article
- Bach1: Function, Regulation, and Involvement in Disease.Oxidative medicine and cellular longevity · 2018Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The acquisition of drug resistance is a persistent clinical problem limiting the successful treatment of glioblastoma (GBM). However, the molecular mechanisms by which initially chemoresponsive tumors develop therapeutic resistance remain poorly understood. In this study, we report that BACH1, a heme-binding protein that participates in transcriptional repression or activation, was significantly upregulated in glioblastoma tissues. Overexpression of BACH1 in GBM cells conferred resistance to temozolomide, whereas its inhibition markedly sensitized resistant cells to temozolomide in vitro and in vivo. Further investigation revealed that BACH1 activation significantly enhanced the expression of MGMT, and depletion of p53 disrupted the effects of BACH1 on MGMT and temozolomide resistance. P53 sequesters SP1 to prevent its binding to the MGMT promoter region and thus inhibits MGMT expression. Moreover, BACH1 overexpression impaired the association between p53 and SP1 via competitive binding p53, and antagonized the impact of p53 on MGMT expression. Finally, we found that BACH1 low expression correlated with better prognosis in GBM patients undergoing temozolomide therapy, especially in patients with wild-type TP53. Collectively, our findings identify a potential mechanism by which wild-type TP53 GBM cells develop resistance to temozolomide and suggest that targeting this pathway may be beneficial for overcoming resistance.
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