Effect of depletion of p53 and BACH1 on gene expression in human tongue squamous cell carcinoma cell line Cal-33.
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE224730 | GEO | 2023/02/15
REPOSITORIES: GEO
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Project description:Effect of depletion of p53 and BACH1 on gene expression in human tongue squamous cell carcinoma cell line Cal-33.
| PRJNA932318 | ENA
Project description:BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements (MAREs) at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAREs, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we combined chromatin immunoprecipitation-sequencing (ChIP-seq) analysis of BACH1 target genes in HEK 293 cells with knock-down of BACH1 using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. The 59 BACH1 target genes identified by ChIP-seq were found highly enriched in genes showing expression changes after BACH1 knock-down, demonstrating the impact of BACH1 repression on transcription. In addition to known and new BACH1 targets involved in heme degradation (HMOX1, FTL, FTH1, ME1, SLC48A1) and redox regulation (GCLC, GCLM, SLC7A11), we also discovered BACH1 target genes effecting cell cycle and apoptosis pathways (ITPR2, CALM1, SQSTM1, TFE3, EWSR1, CDK6, BCL2L11, MAFG) as well as subcellular transport processes (CLSTN1, PSAP, MAPT, vault RNA). The newly identified impact of BACH1 on genes involved in neurodegenerative processes and proliferation provides an interesting basis for future dissection of BACH1-mediated gene repression in neurodegeneration and virus-induced cancerogenesis. Examination of BACH1 binding in HEK 293T cells by chromatin immunoprecipitation-sequencing (CHIP-seq) with input DNA as control.
2011-05-13 | E-GEOD-28051 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE28050: Expression data from knockdown of BACH1 in HEK 293T cells GSE28051: Genome-wide map of BACH1 binding in HEK293T cells Refer to individual Series
2011-05-12 | E-GEOD-28053 | biostudies-arrayexpress
Project description:Genes regulated by Bach1 transcription factor
2012-07-09 | E-MEXP-3674 | biostudies-arrayexpress
Project description:We identify transcription factor BACH1 as a master regulator in vascular cells during aging. BACH1 is upregulated in the aorta of old mice. We find BACH1 is located on open chromatin and BACH1 binds to CDKN1A gene enhancer and activates its transcription in endothelial cells. Finally, BACH1 aggravates endothelial cell senescence under oxidative stress. Thus, these findings demonstrate a crucial regulatory role of BACH1 in vascular aging.
2024-09-15 | GSE185210 | GEO
Project description:BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements (MAREs) at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAREs, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we combined chromatin immunoprecipitation-sequencing (ChIP-seq) analysis of BACH1 target genes in HEK 293 cells with knock-down of BACH1 using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. The 59 BACH1 target genes identified by ChIP-seq were found highly enriched in genes showing expression changes after BACH1 knock-down, demonstrating the impact of BACH1 repression on transcription. In addition to known and new BACH1 targets involved in heme degradation (HMOX1, FTL, FTH1, ME1, SLC48A1) and redox regulation (GCLC, GCLM, SLC7A11), we also discovered BACH1 target genes effecting cell cycle and apoptosis pathways (ITPR2, CALM1, SQSTM1, TFE3, EWSR1, CDK6, BCL2L11, MAFG) as well as subcellular transport processes (CLSTN1, PSAP, MAPT, vault RNA). The newly identified impact of BACH1 on genes involved in neurodegenerative processes and proliferation provides an interesting basis for future dissection of BACH1-mediated gene repression in neurodegeneration and virus-induced cancerogenesis.
2011-05-13 | GSE28051 | GEO
Project description:TP53 R175H mutation is one of the most common mutations in human cancers and cancer cells with this mutation stably express R175H protein in the nucleus. To identify the synthetic lethal gene interacted with the R175H, we conducted the high throughput screening by using tetracyclin inducible R175H expression system in SF126 cells and comprehensive shRNA library carried by lenti virus. We identified 906 candidate gene suppressions that may lead to accelerated cell growth inhibition under the presence of R175H. Inhibitor of differentiation 1 (ID1) was one of the candidate genes and suppression of ID1 by siRNA resulted in acceleration of growth inhibition of cell lines expressing endogenous R175H but not in TP53 null cell lines. The transient expression of R175H in TP53 null cell lines and suppression of ID1 and/or TP53 R175H in cell lines with endogenous R175H revealed that the cell growth inhibition by ID1 suppression was dependent on R175H expression but not other common p53 mutants (R273H). Flow cytometric (FACS) analysis exhibited that ID1 suppression resulted in G1 arrest and the arrest was accelerated by suppression of R175H. In conclusion, ID1 is a synthetic lethal gene interacted with R175H and is considered to be a novel molecular target of cancer therapy for R175H expressing cells. R175H expression(Tet-on) group was labeled by Cy5, and p53-null(Tet-off) group was labeled by Cy3. Three independent experiments were conducted (We have triplicate data).
2011-11-02 | E-GEOD-33362 | biostudies-arrayexpress
Project description:Gain-of-function p53 mutants such as p53-R175H form stable aggregates that accumulate in cells and play an important role in cancer progression. Selective degradation of gain-of-function p53 mutants has emerged as a highly attractive therapeutic strategy to target cancer cells harboring specific p53 mutations. We identified a small molecule called MCB-613 to cause rapid ubiquitination, nuclear export, and degradation of p53-R175H through lysosome-mediated pathway leading to catastrophic cancer cell death. In contrast to its effect on the p53-R175H mutant, MCB-613 causes slight stabilization of p53-WT and has weaker effects on other p53 gain-of-function mutants. Using state-of-the-art genetic and chemical approaches, we identified the deubiquitinase USP15 as the mediator of MCB-613’s effect on p53-R175H and established USP15 as a selective upstream regulator of p53-R175H in ovarian cancer cells. These results confirm that distinct pathways regulate the turnover of p53-WT and the different p53 mutants and open new opportunities to selectively target them.
2018-02-07 | GSE110220 | GEO
Project description:BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements (MAREs) at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAREs, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we performed knock-down of BACH1 in HEK 293T cells using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. Knockdown of BACH1 in HEK 293T cells was carried out with three different types of siRNA molecules (esiRNA = e, siRNA1 SI00309876 from Qiagen = q and Stealth siRNA2 HSS100910 from Invitrogen = s), followed by RNA extraction after 24h and 72h of knockdown and hybridization on Affymetrix microarrays. For each siRNA type, we performed the experiments in triplicates, with four control replicates (mock transfections without siRNA) at 24h and three control replicates at 72h, resulting in nine samples and four controls at 24h and nine samples and three controls at 72h. Samples at 24h of knockdown: e_1_24, e_2_24, e_3_24, q_1_24, q_2_24, q_3_24, s_1_24, s_2_24, s_3_24. Controls at 24h: m_1_24, m_2_24, m_3_24, m_4_72. Samples at 72h of knockdown: e_1_72, e_2_72, e_3_72, q_1_72, q_2_72, q_3_72, s_1_72, s_2_72, s_3_72. Controls at 72h: m_1_72, m_2_72, m_3_72. REPEATS: biological replicate: BACH1_e_1_24, BACH1_e_2_24, BACH1_e_3_24 biological replicate: BACH1_q_1_24, BACH1_q_2_24, BACH1_q_3_24 biological replicate: BACH1_s_1_24, BACH1_s_2_24, BACH1_s_3_24 biological replicate: BACH1_m_1_24, BACH1_m_2_24, BACH1_m_3_24, BACH1_m_4_24 biological replicate: BACH1_e_1_72, BACH1_e_2_72, BACH1_e_3_72 biological replicate: BACH1_q_1_72, BACH1_q_2_72, BACH1_q_3_72 biological replicate: BACH1_s_1_72, BACH1_s_2_72, BACH1_s_3_72 biological replicate: BACH1_m_1_72, BACH1_m_2_72, BACH1_m_3_72
2011-05-13 | E-GEOD-28050 | biostudies-arrayexpress
Project description:The transcription factor BACH1 is a master regulator of human breast cancer metastasis. Here we use gene expression array analysis to identify and compare the genes regulated by BACH1 depletion in a metastatic human breast cancer cell line. Total RNAs were extracted from vector control 1833 cells or 1833 cells with shBACH mRNA BACH1 depletion. Affymetrix GeneChip Human Gene 1.0 ST Arrays were performed to detail the gene expression and identify the genes regulated by BACH1in metastatic human breast cancer cells.
2013-10-31 | E-GEOD-50226 | biostudies-arrayexpress