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GENE:

BACH1 (BTB Domain And CNC Homolog 1)

i
Other names: BTB Domain And CNC Homolog 1, BTB And CNC Homology 1, Basic Leucine Zipper Transcription Factor 1, Transcription Regulator Protein BACH1, BACH-1, BTBD24, Basic Region Leucine Zipper Transcriptional Regulator BACH1, BTB And CNC Homolog 1, HA2303, BACH1
4d
PRMT1 promotes epigenetic reprogramming associated with acquired chemoresistance in pancreatic cancer. (PubMed, Cell Rep)
Cut&Tag chromatin profiling of H3K27Ac, MAFF, and BACH1 suggests a pivotal role for MAFF/BACH1 in global epigenetic response to gemcitabine, which is confirmed by genetically silencing MAFF. PRMT1 and MAFF/BACH1 signature genes identified by Cut&Tag analysis distinguish gemcitabine-resistant from gemcitabine-sensitive patient-derived xenografts of PDAC, supporting the PRMT1-MAFF/BACH1 epigenetic regulatory axis as a potential therapeutic avenue for improving the efficacy and durability of chemotherapies in patients of PDAC.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • PRMT1 (Protein Arginine Methyltransferase 1) • BACH1 (BTB Domain And CNC Homolog 1)
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gemcitabine
8d
TANK Binding Kinase 1 Promotes BACH1 Degradation through Both Phosphorylation-Dependent and -Independent Mechanisms without Relying on Heme and FBXO22. (PubMed, Int J Mol Sci)
Its inhibition in Namalwa B lymphoma cells increased endogenous BACH1 protein. These results suggest that TBK1 promotes BACH1 degradation in parallel to the FBXO22- and heme-dependent pathway, placing BACH1 as a downstream effector of TBK1 in iron metabolism or innate immune response.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1)
1m
Combining bulk and scRNA-seq to explore the molecular mechanisms governing the distinct efferocytosis activities of a macrophage subpopulation in PDAC. (PubMed, J Cell Mol Med)
This observation implies that the diversity of macrophage cells might potentially influence the metastatic advancement of PDAC. Moreover, the central transcription factor of different macrophage subtypes offers a promising opportunity for targeted immunotherapy in the treatment of PDAC.
Journal • IO biomarker
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CD8 (cluster of differentiation 8) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • CD4 (CD4 Molecule) • TGM2 (Transglutaminase 2) • CD68 (CD68 Molecule) • GAS6 (Growth arrest specific 6) • ITGAM (Integrin, alpha M) • BACH1 (BTB Domain And CNC Homolog 1) • TEAD4 (TEA Domain Transcription Factor 4)
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TGM2 expression
2ms
Identification of BACH1-IT2-miR-4786-Siglec-15 immune suppressive axis in bladder cancer. (PubMed, BMC Cancer)
The BACH1-IT2-miR-4786-Siglec-15 axis significantly influences activation of immune cell co-culture. In summary, our data highlights the critical involvements of BACH1-IT2 and miR-4786 in immune evasion in bladder cancer, which hints the potential for both therapeutic and prognostic exploitation.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1) • SIGLEC15 (Sialic Acid Binding Ig Like Lectin 15)
2ms
Bile acids inhibit ferroptosis sensitivity through activating farnesoid X receptor in gastric cancer cells. (PubMed, World J Gastroenterol)
This study revealed for the first time that BAs could inhibit ferroptosis sensitivity through the FXR-BACH1-GSH-GPX4 axis in GC cells. This work provided new insights into the mechanism associated with BA-mediated promotion of GC and may help identify potential therapeutic targets for GC patients with BAs reflux.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • GPX4 (Glutathione Peroxidase 4) • BACH1 (BTB Domain And CNC Homolog 1)
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GPX4 expression • BACH1 overexpression
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erastin
3ms
Transcription factor BACH1 in cancer: roles, mechanisms, and prospects for targeted therapy. (PubMed, Biomark Res)
Finally, the promising directions of future BACH1 research are prospected. A systematical and clear understanding of BACH1 would undoubtedly take us one step closer to facilitating its translation from basic research into the clinic.
Review • Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1)
3ms
Gene signatures associated with prognosis and chemotherapy resistance in glioblastoma treated with temozolomide. (PubMed, Front Genet)
PADI4, SDF4, and TP53INP1 are novel therapy and biomarker candidates for GBM. Further investigation of their oncologic functions may provide new insight into GBM treatment resistance mechanisms.
Journal • Gene Signature
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1) • CDKN2C (Cyclin Dependent Kinase Inhibitor 2C) • IFI16 (Interferon Gamma Inducible Protein 16) • TP53INP1 (Tumor Protein P53 Inducible Nuclear Protein 1)
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temozolomide
4ms
Sanguinarine chloride induces ferroptosis by regulating ROS/BACH1/HMOX1 signaling pathway in prostate cancer. (PubMed, Chin Med)
This study provides evidence that S.C effectively suppresses tumor progression and induces ferroptosis in prostate cancer cells by targeting the ROS/USP47/BACH1/HMOX1 axis. These findings offer novel insights into the underlying mechanism by which S.C inhibits the progression of prostate cancer. Furthermore, leveraging the potential of S.C in targeting ferroptosis may present a new therapeutic opportunity for prostate cancer. This study found that S.C induces ferroptosis by targeting the ROS/USP47/BACH1/HMOX1 axis in prostate cancer cells.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • HMOX1 (Heme Oxygenase 1) • BACH1 (BTB Domain And CNC Homolog 1) • USP47 (Ubiquitin Specific Peptidase 47)
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HMOX1 expression
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docetaxel
5ms
Measuring the Effects of Talazoparib in Patients With Advanced Cancer and DNA Repair Variations (clinicaltrials.gov)
P2, N=36, Recruiting, National Cancer Institute (NCI) | Trial completion date: Dec 2023 --> Dec 2024 | Trial primary completion date: Dec 2023 --> Dec 2024
Trial completion date • Trial primary completion date • Metastases
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BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • ARID1A (AT-rich interaction domain 1A) • BAP1 (BRCA1 Associated Protein 1) • CDK12 (Cyclin dependent kinase 12) • CHEK2 (Checkpoint kinase 2) • RAD51 (RAD51 Homolog A) • FANCA (FA Complementation Group A) • RAD51B (RAD51 Paralog B) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • RAD51C (RAD51 paralog C) • RAD50 (RAD50 Double Strand Break Repair Protein) • RAD51D (RAD51 paralog D) • CHEK1 (Checkpoint kinase 1) • BARD1 (BRCA1 Associated RING Domain 1) • NBN (Nibrin Nijmegen Breakage Syndrome 1 (Nibrin)) • RAD54L (DNA Repair And Recombination Protein RAD54) • FANCF (FA complementation group F) • FANCL (FA Complementation Group L) • FANCI (FA Complementation Group I) • FANCM (FA Complementation Group M) • BACH1 (BTB Domain And CNC Homolog 1) • FANCD2 (FA Complementation Group D2) • FANCE (FA Complementation Group E) • FANCG (FA Complementation Group G) • FANCB (FA Complementation Group B) • FANCC (FA Complementation Group C)
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BRCA2 mutation • BRCA1 mutation • ATM mutation
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Talzenna (talazoparib)
5ms
BACH1 loss exerts antitumor effects on mantle cell lymphoma cells via inducing a tumor-intrinsic innate immune response and cell cycle arrest. (PubMed, Mol Cancer Res)
Further double-knockdown functional assays confirmed that loss of BACH1 induced ZBTB20-mediated IFN-α production and HBP1-mediated cell-cycle arrest, indicating that BACH1-centered regulatory network may be a novel targetable vulnerability in MCL cells. Implications: BACH1 serves as a pleotropic regulator of tumor-intrinsic innate immune response and cell-cycle progression, disruption of which may offer a promising therapeutic strategy for MCL treatment.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1) • IFNA1 (Interferon Alpha 1) • HBP1 (HMG-Box Transcription Factor 1)
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BACH1 overexpression
5ms
α-Pyrrolidinononanophenone derivatives induce differentiated SH-SY5Y neuroblastoma cells apoptosis via reduction of antioxidant capacity: Involvement of NO depletion and inactivation of Nrf2/HO1 signaling pathway. (PubMed, Neurotoxicology)
Additionally, pretreatment with an NO donor suppresses the I-α-PNP-evoked ROS overproduction, HO1 down-regulation, increased nuclear Bach1 expression and reduced antioxidant activity in the differentiated cells. These findings suggest that the ROS-dependent apoptosis by I-α-PNP in differentiated cells is attributed to the inactivation of the Nrf2/HO1 signaling pathway triggered by NO depletion.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • HMOX1 (Heme Oxygenase 1) • GPX4 (Glutathione Peroxidase 4) • BACH1 (BTB Domain And CNC Homolog 1)
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GPX4 expression • HMOX1 expression
5ms
Circ_0005015 upregulates BACH1 to promote aggressive behaviors in glioblastoma by sponging microRNA-382-5p. (PubMed, Naunyn Schmiedebergs Arch Pharmacol)
In addition, circ_0005015 knockdown might repress tumor growth in vivo. Circ_0005015 boosted GBM progression via binding to miR-382-5p to up-regulate BACH1, which may offer new effective targets for GBM treatment.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • MMP9 (Matrix metallopeptidase 9) • PCNA (Proliferating cell nuclear antigen) • BACH1 (BTB Domain And CNC Homolog 1)
6ms
A systems-level analysis of the mutually antagonistic roles of RKIP and BACH1 in dynamics of cancer cell plasticity. (PubMed, J R Soc Interface)
Finally, we observed that low RKIP levels and upregulated BACH1 levels associated with worse clinical outcomes in many cancer types. Together, our systems-level analysis indicates that the emergent dynamics of underlying regulatory network enable the antagonistic patterns of RKIP and BACH1 with various axes of cancer cell plasticity, and with patient survival data.
Journal
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PD-L1 (Programmed death ligand 1) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1)
6ms
Gene expression profiles to analyze the anticancer and carcinogenic effects of arsenic in bladder cancer. (PubMed, Am J Transl Res)
Arsenic exerted carcinogenic and anticancer functions by altering the expression of crosstalk genes such as BDKRB2, FOS, NR4A1, PLAU, SH3BGRL, and F10, and these were due to arsenic binding proteins.
Journal • Gene Expression Profile • PARP Biomarker
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KRAS (KRAS proto-oncogene GTPase) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • PARP1 (Poly(ADP-Ribose) Polymerase 1) • LTBP1 (Latent-transforming growth factor beta-binding protein 1) • BACH1 (BTB Domain And CNC Homolog 1) • NR4A1 (Nuclear Receptor Subfamily 4 Group A Member 1) • SH3BGRL (SH3 Domain Binding Glutamate Rich Protein Like) • PLAU (Plasminogen Activator) • ZFP36 (ZFP36 Ring Finger Protein)
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arsenic trioxide
6ms
Lnc AC016727.1/BACH1/HIF-1 α signal loop promotes the progression of non-small cell lung cancer. (PubMed, J Exp Clin Cancer Res)
Our study reveals a novel lncRNA AC016727.1/BACH1/HIF-1α signaling loop in the progression of NSCLC under hypoxic conditions, suggesting that lncRNA AC016727.1 could act as a useful biomarker for NSCLC and a new therapeutic target.
Journal
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HIF1A (Hypoxia inducible factor 1, alpha subunit) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1) • MIR98 (MicroRNA 98)
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HIF1A expression
6ms
Extracellular Vesicles Secreted from Daratumumab Resistant Cells Promote Resistance and Proliferation of Daratumumab Sensitive Cells, Possibly through the Transfer of miRNA Cargo (ASH 2023)
Here, we highlight that the enriched expression of exosome pathway proteins reported in dara R cell lines is not detected in Lenalidomide or Bortezomib-resistant cell lines, or in other monoclonal antibody resistant cell lines such as anti-CD20 (Rituximab)-resistant cell lines, thus indicating that this mechanism is unique to daratumumab resistance...Next, we assessed the effect of inhibiting dara R EV secretion by applying Neticonazole and Ketoconazole, prior to coculture of resistant and sensitive cell lines...We are currently elucidating the biological basis for dara resistance mediated by these miRNAs. A deeper understanding of the mechanisms involved may pave the way for clinical evaluation of EV- directed therapeutics to overcome dara resistance.
IO biomarker
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • MIR155 (MicroRNA 155) • BACH1 (BTB Domain And CNC Homolog 1) • JARID2 (Jumonji And AT-Rich Interaction Domain Containing 2) • CD81 (CD81 Molecule) • MIR181A1 (MicroRNA 181a-1)
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miR-155 expression
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Rituxan (rituximab) • lenalidomide • bortezomib • Darzalex (daratumumab)
7ms
Antioxidants stimulate BACH1-dependent tumor angiogenesis. (PubMed, J Clin Invest)
BACH1 is stabilized by lowering ROS levels; consequently, angiogenesis gene expression in lung cancer cells, tumor organoids, and xenograft tumors increased substantially following administration of vitamins C and E and N-acetylcysteine in a BACH1-dependent fashion under normoxia...BACH1 expression in tumor sections from lung cancer patients correlates with angiogenesis gene and protein expression. We conclude that BACH1 is an oxygen- and redox-sensitive angiogenesis transcription factor.
Journal
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HIF1A (Hypoxia inducible factor 1, alpha subunit) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1)
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HIF1A expression • BACH1 overexpression
7ms
Prognostic Worth of Nrf2/BACH1/HO-1 Protein Expression in the Development of Breast Cancer. (PubMed, Med Princ Pract)
Nrf2, BACH1 and HO-1 could be explored as a biomarker for cancer stage, progression, and prognosis.
Journal
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HER-2 (Human epidermal growth factor receptor 2) • PGR (Progesterone receptor) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1)
7ms
Evaluation of Rapanone and Nectandrin B as novel inhibitors for targeting the metastatic regulator protein BACH1 using breast cancer cell line Mcf-7. (PubMed, J Biomol Struct Dyn)
The two plant origin compounds Rapanone and Nectandrin B might be novel candidates for developing anti-cancer drugs. The predicted compounds were further validated through in-vitro experimental approaches.Communicated by Ramaswamy H. Sarma.
Preclinical • Journal • Metastases
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1)
8ms
Formononetin enhances the chemosensitivity of triple negative breast cancer via BTB domain and CNC homolog 1-mediated mitophagy pathways. (PubMed, Acta Biochim Pol)
Taken together, FM suppressed the aggressiveness of TNBC via BACH1/p53 signaling. Therefore, FM may be an alternative strategy for TNBC.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1)
8ms
BACH1 promotes lung adenocarcinoma cell metastasis through transcriptional activation of ITGA2. (PubMed, Cancer Sci)
Mechanistically, BACH1 directly binds to the upstream sequence of the ITGA2 promoter to promote ITGA2 expression, and the BACH1-ITGA2 axis is involved in cytoskeletal regulation in lung adenocarcinoma cells by activating the FAK-RAC1-PAK signaling pathway. Our results indicated that BACH1 positively regulates the expression of ITGA2 through a transcriptional mechanism, thereby activating the FAK-RAC1-PAK signaling pathway to participate in the formation of the cytoskeleton in tumor cells and then promoting the migration and invasion of tumor cells.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1) • ITGA2 (Integrin Subunit Alpha 2)
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BACH1 overexpression
9ms
Hyperforin Enhances Heme Oxygenase-1 Expression Triggering Lipid Peroxidation in BRAF-Mutated Melanoma Cells and Hampers the Expression of Pro-Metastatic Markers. (PubMed, Antioxidants (Basel))
We observed the decreased expression of CD133, octamer-4, tyrosine-kinase receptor AXL, urokinase plasminogen activator receptor, and metalloproteinase-2 following HPF treatment. These findings provide further support for our previous observations, demonstrating the inhibitory effects of HPF on cell motility and colony formation in soft agar, which are both metastasis-related processes in tumor cells.
Journal • Metastases
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BRAF (B-raf proto-oncogene) • AXL (AXL Receptor Tyrosine Kinase) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • HMOX1 (Heme Oxygenase 1) • GPX4 (Glutathione Peroxidase 4) • NTRK (Neurotrophic receptor tyrosine kinase) • SLC7A11 (Solute Carrier Family 7 Member 11) • BACH1 (BTB Domain And CNC Homolog 1)
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BRAF mutation • CD133 expression • HMOX1 expression
10ms
Chemotherapy-induced exosomal circBACH1 promotes breast cancer resistance and stemness via miR-217/G3BP2 signaling pathway. (PubMed, Breast Cancer Res)
These results demonstrated that PTX-induced exosomal circBACH1 promoted stemness and migration of BC cells by sponging miR-217 to upregulate the expression of G3BP2, which provided a new therapeutic target for PTX-resistance and progression of BC via circBACH1/miR-217/G3BP2 axis.
Journal
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BACH1 (BTB Domain And CNC Homolog 1) • G3BP2 (G3BP Stress Granule Assembly Factor 2) • MIR217 (MicroRNA 217)
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paclitaxel
10ms
The possible molecular mechanism underlying the involvement of the variable shear factor QKI in the epithelial-mesenchymal transformation of oesophageal cancer. (PubMed, PLoS One)
Variable shear factor QKI promotes hsa_circ_0006646 and hsa_circ_0061395 generation, and downstream related miRNAs can relieve the targeted inhibition of EMT-related genes (IL11, MFAP2, MMP10, MMP1) and promote the occurrence and development of oesophageal cancer, providing a new theoretical basis for screening prognostic markers of oesophageal cancer patients.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • QKI (QKI, KH Domain Containing RNA Binding) • BACH1 (BTB Domain And CNC Homolog 1) • MMP1 (Matrix metallopeptidase 1) • PTK2 (Protein Tyrosine Kinase 2)
10ms
BACH1 encourages ferroptosis by activating KDM4C-mediated COX2 demethylation after cerebral ischemia-reperfusion injury. (PubMed, Eur J Neurosci)
In vivo findings displayed that brain infraction, pathological damage, and neuronal loss rate in middle cerebral artery occlusion (MCAO) mice were conspicuously decreased after BACH1 knock-down. This study reveals that BACH1 encourages ferroptosis in neuroblastoma cells and CIRI mouse brain tissues by activating KDM4C-mediated COX2 demethylation.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • GPX4 (Glutathione Peroxidase 4) • PTGS2 (Prostaglandin-Endoperoxide Synthase 2) • SLC7A11 (Solute Carrier Family 7 Member 11) • BACH1 (BTB Domain And CNC Homolog 1) • MT-CO2 (Mitochondrially Encoded Cytochrome C Oxidase II)
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PTGS2 expression
10ms
Nonmonotone invasion landscape by noise-aware control of metastasis activator levels. (PubMed, Nat Chem Biol)
Additionally, BACH1's expression variability aids invasion at high BACH1 expression. Overall, precisely engineered, noise-aware protein-level control is necessary and important to unravel disease effects of genes to improve clinical drug efficacy.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1)
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BACH1 overexpression
10ms
Oncolytic virus • IO biomarker
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1)
11ms
USP14 regulates heme metabolism and ovarian cancer invasion through BACH1 deubiquitination and stabilization. (PubMed, Biochem Biophys Res Commun)
The depletion of BACH1 or inhibition of heme oxygenase 1 (coded by HMOX-1) was also found to significantly impair USP14-dependent OV cell invasion. In conclusion, our results highlight the importance of the NRF2-USP14-BACH1 axis in regulating OV cell invasion and heme metabolism, providing evidence for its potential as a therapeutic target in related diseases.
Journal
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NFE2L2 (Nuclear Factor, Erythroid 2 Like 2) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • HMOX1 (Heme Oxygenase 1) • BACH1 (BTB Domain And CNC Homolog 1) • USP14 (Ubiquitin Specific Peptidase 14)
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HMOX1 expression
12ms
Pathophysiological role of BACH transcription factors in digestive system diseases. (PubMed, Front Physiol)
Additionally, we summarize a list of regulators targeting these proteins. Our review provides a reference for future studies on targeted drugs in digestive diseases.
Review • Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1) • BACH2 (BTB Domain And CNC Homolog 2)
12ms
Ferroptosis model system by the re-expression of BACH1. (PubMed, J Biochem)
Furthermore, we confirmed that the ferroptosis induced by BACH1 re-expression exhibited a propagating effect. BACH1 re-expression represents a new strategy for inducing ferroptosis after GPX4 or system Xc- suppression, and is expected to contribute to future ferroptosis research.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • GPX4 (Glutathione Peroxidase 4) • BACH1 (BTB Domain And CNC Homolog 1) • AIFM2 (Apoptosis Inducing Factor Mitochondria Associated 2)
1year
Thioredoxin facilitates hepatocellular carcinoma stemness and metastasis by increasing BACH1 stability to activate the AKT/mTOR pathway. (PubMed, FASEB J)
Furthermore, we found that the specific inhibition of TXN in combination with lenvatinib in mice significantly improved the treatment of metastatic HCC. In summary, our data demonstrate that TXN plays a crucial role in HCC stemness and BACH1 plays an integral part in regulating this process by activating the AKT/mTOR pathway. Thus, TXN is a promising target for metastatic HCC therapy.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • TXN (Thioredoxin) • BACH1 (BTB Domain And CNC Homolog 1)
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Lenvima (lenvatinib)
1year
DNA DAMAGE RECOVERY AND CHEMOSENSITIVITY TO OLAPARIB AND CISPLATIN IN BREAST CANCER CELLS WITH MUTATION ON BRCT DOMAIN OF BRCA1 PROTEIN (GBCC 2023)
The mechanism of response to DNA break and chemosensitivity of breast cancer cells are possibly influenced by the location of BRCA1 mutation. To find the prognostic and predictive meaning of these characteristic, well-controlled preclinical and clinical studies are needed.
BRCA Biomarker • PARP Biomarker
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BRCA1 (Breast cancer 1, early onset) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1)
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BRCA1 mutation • BRCA wild-type • BRIP1 mutation
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Lynparza (olaparib) • cisplatin
1year
Epigenetic regulation of HBV-specific tumor infiltrating T cells in HBV-related HCC. (PubMed, Hepatology)
This study provides insight into the cellular and molecular basis of the epigenomic programs that regulate the differentiation and generation of HBV-related T cells from viral infection and HBV + HCC unique immune exhaustion.
Journal
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CD8 (cluster of differentiation 8) • CTLA4 (Cytotoxic T-Lymphocyte Associated Protein 4) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • NFKB1 (Nuclear factor of kappa light polypeptide gene enhancer in B-cells 1) • BACH1 (BTB Domain And CNC Homolog 1)
1year
ROS-lowering doses of vitamins C and A accelerate malignant melanoma metastasis. (PubMed, Redox Biol)
Consequently, reducing oxidative stress with the antioxidant N-acetylcysteine (NAC) stimulates melanoma cell migration in vitro and metastasis in vivo...Genomics analyses revealed that the transcription factor BACH1 is activated following antioxidant administration and knockout of Bach1 in mouse melanoma cells reduced lymph node and liver metastasis in xenograft mouse models. We conclude that a broad range of antioxidants accelerate melanoma migration and metastasis and that BACH1 is functionally linked to melanoma metastasis in vivo.
Journal
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BRAF (B-raf proto-oncogene) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1)
1year
FBXO22 promotes leukemogenesis by targeting BACH1 in MLL-rearranged acute myeloid leukemia. (PubMed, J Hematol Oncol)
FBXO22 promotes MLLr AML progression by targeting BACH1 and targeting FBXO22 might be an ideal strategy to eradicate LSCs without influencing normal hematopoiesis.
Journal
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BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1)
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MLL rearrangement • BACH1 overexpression
over1year
A Trial of Niraparib in BAP1 and Other DNA Damage Response (DDR) Deficient Neoplasms (UF-STO-ETI-001) (clinicaltrials.gov)
P2, N=35, Completed, University of Florida | Active, not recruiting --> Completed | Trial completion date: Dec 2023 --> Aug 2022 | Trial primary completion date: Dec 2022 --> Aug 2022
Trial completion • Trial completion date • Trial primary completion date
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PTEN (Phosphatase and tensin homolog) • IDH1 (Isocitrate dehydrogenase (NADP(+)) 1) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • ARID1A (AT-rich interaction domain 1A) • BAP1 (BRCA1 Associated Protein 1) • CDK4 (Cyclin-dependent kinase 4) • CHEK2 (Checkpoint kinase 2) • RAD51 (RAD51 Homolog A) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • POLD1 (DNA Polymerase Delta 1) • RAD50 (RAD50 Double Strand Break Repair Protein) • CHEK1 (Checkpoint kinase 1) • BARD1 (BRCA1 Associated RING Domain 1) • NBN (Nibrin Nijmegen Breakage Syndrome 1 (Nibrin)) • CDK2 (Cyclin-dependent kinase 2) • WRN (WRN RecQ Like Helicase) • RAD52 (RAD52 Homolog DNA Repair Protein) • BACH1 (BTB Domain And CNC Homolog 1) • FANCG (FA Complementation Group G) • PRKDC (Protein Kinase, DNA-Activated, Catalytic Subunit) • RPA1 (Replication Protein A1) • ABRAXAS1 (Abraxas 1 BRCA1 A Complex Subunit 2) • FEN1 (Flap Structure-Specific Endonuclease 1) • SLX4 (SLX4 Structure-Specific Endonuclease Subunit)
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BARD1 mutation • WRN mutation • RPA1 mutation
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Zejula (niraparib)
over1year
Ryanodine receptor 2 promotes colorectal cancer metastasis by the ROS/BACH1 axis. (PubMed, Mol Oncol)
RyR2 regulates cellular reactive oxygen species (ROS) levels, which activates nuclear factor erythroid 2-related factor 2 (Nrf2; also known as NFE2L2) and HMOX1 expression, and thus BACH1 accumulation. Collectively, this study provides evidence that the RyR2/ROS/BACH1 axis may be a potential target to intervene with CRC metastasis.
Journal
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KRAS (KRAS proto-oncogene GTPase) • NFE2L2 (Nuclear Factor, Erythroid 2 Like 2) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • HMOX1 (Heme Oxygenase 1) • BACH1 (BTB Domain And CNC Homolog 1)
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KRAS mutation • HMOX1 expression • KRAS expression
over1year
UBR7 inhibits HCC tumorigenesis by targeting Keap1/Nrf2/Bach1/HK2 and glycolysis. (PubMed, J Exp Clin Cancer Res)
These results collectively establish UBR7 as a critical negative regulator of aerobic glycolysis and HCC tumorigenesis through regulation of the Keap1/Nrf2/Bach1/HK2 axis, providing a potential clinical and therapeutic target for the HCC treatment.
Journal
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KEAP1 (Kelch Like ECH Associated Protein 1) • BRIP1 (BRCA1 Interacting Protein C-terminal Helicase 1) • BACH1 (BTB Domain And CNC Homolog 1) • H2BC8 (H2B Clustered Histone 8) • ALKBH5 (AlkB Homolog 5, RNA Demethylase)
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KEAP1 expression