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BCL6 mediates Chemoresistance in Acute Myeloid Leukemia

ABSTRACT: BCL6 mediates Chemoresistance in Acute Myeloid Leukemia

PROVIDER: PRJNA549958 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9332931_1.fastq.gz	Fastqsanger.gz
	SRR9332931_2.fastq.gz	Fastqsanger.gz
	SRR9332932_1.fastq.gz	Fastqsanger.gz
	SRR9332932_2.fastq.gz	Fastqsanger.gz
	SRR9332933_1.fastq.gz	Fastqsanger.gz

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BCL6 mediates Chemoresistance in Acute Myeloid Leukemia

Project description:BCL6 is a transcription repressor that plays a crucial role in germinal center formation and lymphomagenesis. However, its role in myeloid malignancies remains unclear. Here, we explored the role of BCL6 in acute myeloid leukemia (AML). Heterogeneous levels of BCL6 were found across AML cell lines and primary AML samples. Cells with higher levels of BCL6 were indeed sensitive to treatment with BCL6 inhibitors. Gene expression profiling of AML cells treated with BCL6 inhibitor revealed a subset of target genes that are common with lymphoma cells. Ex vivo treatment of primary AML cells with BCL6 peptide inhibitor (BPI) induced apoptosis and decrease colony forming capacity which correlated with the levels of BCL6 expression . Importantly, inhibition of BCL6 in primary AML cells with either BPI or BCL6 siRNA resulted in significant reduction of leukemia initiating capacity using immunodeficient mice, suggesting ablation of leukemia stem cells (LSC). Such anti-LSC activity was also observed as downregulation of LSC gene signatures using gene expression analyses of cells treated with a BCL6 inhibitor. Importantly, treatment with cytarabine (AraC) induced BCL6 expression, and the levels of BCL6 induction were correlated with resistance to AraC. Treatment of AML primary derived xenografts (PDX) revealed that when AraC was combined with BCL6 inhibitor, inhibition of BCL6 significantly potentiated the efficacy of AraC and improved cytotoxic effects by interfering with the leukemia initiating capacity of AML cells. This suggests that pharmacological inhibition of BCL6 might provide a novel therapeutic strategy for ablation of LSCs and overcome chemoresistance in AML.

2020-08-01 | GSE133112 | GEO

BCL6 is required for the initiation and maintenance of chronic myeloid leukemia

Project description:We identified the BCL6 protooncogene as a critical downstream effector of FoxO3A in self-renewal signaling of CML-initiating cells. BCL6 represses Arf and p53 in CML cells and is required for leukemia stem cell maintenance, colony formation and initiation of leukemia in transplant recipients. Importantly, peptide inhibition of BCL6 in human CML cells compromises colony formation and leukemia-initiation in xenotransplanted mouse recipients. These findings identify peptide-inhibition of BCL6 as a novel strategy to eradicate leukemia-initiating cells in CML. Identification of BCL6 binding sites in human CML cell line JURL-MK1

2011-09-15 | E-GEOD-26085 | biostudies-arrayexpress

BCL6 is required for the initiation and maintenance of chronic myeloid leukemia

2011-09-15 | GSE26085 | GEO

Chemoresistance in acute myeloid leukemia: a single-cell RNA sequencing approach

Project description:Chemoresistance in acute myeloid leukemia: a single-cell RNA sequencing approach

| PRJNA816449 | ENA

Myeloid Leukemia

Project description:Myeloid Leukemia

| PRJNA941283 | ENA

Targeting STAT3-Mediated Lipid Metabolism Reprogramming Overcomes Chemoresistance in Acute Myeloid Leukemia

Project description:Targeting STAT3-Mediated Lipid Metabolism Reprogramming Overcomes Chemoresistance in Acute Myeloid Leukemia

| PRJNA1451102 | ENA

Reciprocal leukemia-stroma VCAM-1/VLA-4-dependent activation 1 of NF-ÎºB mediates chemoresistance

Project description:Bone marrow (BM) mesenchymal stromal cells (BM-MSC) upregulate their NF-ÎºB signaling to protect leukemia cells from chemotherapy-induced apoptosis. To elucidate molecular mechanisms by which leukemia-stroma interactions within the BM microenvironment could confer chemoresistance to leukemia cells, we used genome-wide gene expression profiling (GEP) to examine human normal BM-MSC that had been co-cultured with the pre-B ALL REH cells and then separated by flow cytometry (FACS). GEP results for co-cultured cells of each type were compared to GEP results for cells of the corresponding type cultured alone, and taken through the same FACS purification procedure, to identify changes in gene expression profiles caused by co-culture.

2014-05-19 | E-GEOD-55533 | biostudies-arrayexpress

Gilteritinib-induced upregulation of S100A9 is mediated through BCL6 in Acute Myeloid Leukemia

Project description:Gilteritinib-induced upregulation of S100A9 is mediated through BCL6 in Acute Myeloid Leukemia

| PRJNA743665 | ENA

Targeting STAT3-Mediated Lipid Metabolism Reprogramming Overcomes Chemoresistance in Acute Myeloid Leukemia

Project description:Chemotherapy resistance and intolerance pose significant challenges in the effective treatment of leukemia. Among the distinctive features associated with chemoresistance, metabolic reprogramming emerges as a key factor. In this study, we unveil a novel mechanism contributing to chemoresistance in leukemia, specifically highlighting the pivotal role of altered lipid homeostasis.We found that multiple lipid metabolism processes are aberrantly activated in Ara-C resistant AML cells, with upregulation of JAK-STAT3 signaling pathways and multiple enzymes in the process of fatty acid metabolism. A potent, and highly selective STAT3 inhibitor, W1307, was designed, and exhibited significant anti-tumor activities in vitro and in vivo. Genetic and pharmacological inhibition of STAT3 leads to inhibition of lipid synthesis and catabolism, resulting lipids metabolic disorder. Mechanistically, STAT3 binds to consensus DNA response elements in the promoters of the lipid metabolism associated genes (SREBP1, CPT2) and regulates their expression. Furthermore, inhibition of STAT3 enhances the anti-tumor effect of Ara-C and sensitizes resistant AML cell line to Ara-C through disrupting lipid homeostasis and triggering lipotoxicity. Collectively, our work illuminates the pivotal role of lipid metabolism adaptation driven by STAT3 in chemoresistance. The identification of W1307 as a promising candidate compound underscores its potential as a therapeutic intervention in leukemia treatment and overcoming chemoresistance.

2026-04-14 | GSE327495 | GEO

Gene expression data of BCR-ABL1 transformed myeloid cells from BCL6 wild-type and BCL6 knockout mice treated with and without Imatinib and RI-BPI

Project description:To identify differences in the gene regulation between BCL6+/+ and BCL6-/- CML cells a gene expression analysis has been performed. We investigated the gene expression pattern in BCL6+/+ cells in the presence or absence of Imatinib and a combination of Imatinib and RI-BPI (a novel retro-inverso BCL6 peptide inhibitor). In BCL6-/- CML cells, we investigated the gene expression pattern in the presence or absence of Imatinib. BCR-ABL1 transformed myeloid cells from BCL6+/+ mice were cultured in the presence or absence of 10µM Imatinib or 10µM Imatinib and 20µM RI-BPI for 16 hours. BCR-ABL1 transformed myeloid cells from BCL6-/- mice were cultured in the presence or absence of 10µM Imatinib. Two samples for each condition were processed.

2011-08-23 | E-GEOD-24813 | biostudies-arrayexpress

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