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BPTF inhibitor increases gastric cancer response to Erlotinib by epigenetically regulating c-MYC/PLCG1/pErk axis.

ABSTRACT: BPTF inhibitor increases gastric cancer response to Erlotinib by epigenetically regulating c-MYC/PLCG1/pErk axis.

PROVIDER: PRJNA823552 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18636191_1.fastq.gz	Fastqsanger.gz
	SRR18636191_2.fastq.gz	Fastqsanger.gz
	SRR18636192_1.fastq.gz	Fastqsanger.gz
	SRR18636192_2.fastq.gz	Fastqsanger.gz
	SRR18636193_1.fastq.gz	Fastqsanger.gz

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BPTF inhibitor increases gastric cancer response to Erlotinib by epigenetically regulating c-MYC/PLCG1/pErk axis [RNA-seq]

Project description:To understand how BPTF conferred resistance to Erlotinib in GC cells, we performed transcriptome profiling (RNA-seq) in MGC803/BPTF-KO and MGC803/BPTF-NC cells.

2023-12-13 | GSE200182 | GEO

BPTF inhibitor increases gastric cancer response to Erlotinib by epigenetically regulating c-MYC/PLCG1/pErk axis [ChIP-seq]

Project description:BPTF inhibitor increases gastric cancer response to Erlotinib by epigenetically regulating c-MYC/PLCG1/pErk axis [ChIP-seq]

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BPTF inhibitor increases gastric cancer response to Erlotinib by epigenetically regulating c-MYC/PLCG1/pErk axis [RNA-seq]

Project description:BPTF inhibitor increases gastric cancer response to Erlotinib by epigenetically regulating c-MYC/PLCG1/pErk axis [RNA-seq]

| PRJNA823562 | ENA

BPTF inhibitor increases gastric cancer response to Erlotinib by epigenetically regulating c-MYC/PLCG1/pErk axis [ChIP-seq]

Project description:Chromatin immunoprecipitation with massively parallel DNA sequencing (ChIP-Seq) was performed by using the anti-BPTF antibody in MGC803 cells to explore the downstream target genes of BPTF.

2023-12-13 | GSE200181 | GEO

BPTF inhibitor increases gastric cancer response to Erlotinib by epigenetically regulating c-MYC/PLCG1/pErk axis.

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-12-13 | GSE200183 | GEO

BPTF Drives Gastric Cancer Resistance to EGFR Inhibitor by Epigenetically Regulating the C-MYC/PLCG1/Perk Axis.

Project description:Erlotinib, an EGFR tyrosine kinase inhibitor, is used for treating patients with cancer exhibiting EGFR overexpression or mutation. However, the response rate of erlotinib is low among patients with gastric cancer (GC). The findings of this study illustrated that the overexpression of bromodomain PHD finger transcription factor (BPTF) is partially responsible for erlotinib resistance in GC, and the combination of the BPTF inhibitor AU-1 with erlotinib synergistically inhibited tumor growth both in vivo and in vitro. AU-1 inhibited the epigenetic function of BPTF and decreased the transcriptional activity of c-MYC on PLCG1 by attenuating chromosome accessibility of the PLCG1 promoter region, thus decreasing the expression of p-PLCG1 and p-Erk and eventually improving the sensitivity of GC cells to erlotinib. In patient-derived xenograft (PDX) models, AU-1 monotherapy exhibited remarkable tumor-inhibiting activity and is synergistic anti-tumor effects when combined with erlotinib. Altogether, the findings illustrate that BPTF affects the responsiveness of GC to erlotinib by epigenetically regulating the c-MYC/PLCG1/pErk axis, and the combination of BPTF inhibitors and erlotinib is a viable therapeutic approach for GC.

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AML1-ETO induced leukemia stem cell self-renewal depends on Plcg1

Project description:Leukemia stem cells are characterized by aberrant self-renewal capacity. Targeting oncogenic fusions that mediate this aberrant self-renewal capacity remains a therapeutic challenge. The t(8;21) translocation, resulting in the oncogenic fusion AML1-ETO (AE, RUNX1-RUNXT1) is among the most common chromosomal rearrangements found in acute myeloid leukemia (AML). By conducting high-resolution proteomic analysis on myeloid leukemia stem cells we identified Phospholipase C- and Ca++-signaling pathways to be differentially regulated in AE/t(8;21) AML. Phospholipase C gamma 1 (Plcg1) was specifically, and highly expressed in t(8;21) AML and could be identified as a direct target of the AML1(RUNX1)-ETO fusion. Genetic inactivation of Plcg1 resulted in abrogation of disease initiation by AE, reduction of intracellular Ca++ release and loss of AE-driven self-renewal programs. Plcg1 deletion after onset of AE-induced leukemia significantly reduced disease penetrance, number of leukemia stem cells and resulted in abrogation of leukemia development in secondary recipients. Inactivation of Plcg1 in human AE-positive AML cells by RNAi reduced colony formation and AML development in vivo. In contrast, Plcg1 was dispensable for steady state hematopoiesis and maintenance of murine and human hematopoietic stem cells (HSC). Translationally, we used pharmacologic inhibition of Ca++ signaling downstream of Plcg1 in AE-driven AML and this resulted in impaired proliferation and self-renewal capacity. The Plcg1 pathway represents a novel, specific vulnerability of AE-driven leukemia and represents an important new therapeutic target.

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AML1-ETO induced leukemia stem cell self-renewal depends on Plcg1

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BPTF is required for c-MYC-induced remodelling of target chromatin and transcriptional activation [RNA-Seq]

Project description:The c-MYC oncogene is a key transcription factor deregulated in most human tumors. Histone marks associated with transcriptionally active genes in euchromatic islands define the set of high-affinity c-MYC targets. The mechanisms involved in their recognition by c-MYC are not known but likely involve chromatin-remodelling and chromatin-modifying complexes. Here, we show that c-MYC interacts with BPTF, a core subunit of the NURF complex that binds active chromatin. BPTF is required for the activation of the full c-MYC transcriptional programme in fibroblasts. BPTF knockdown leads to a decrease in c-MYC recruitment to DNA and to changes in chromatin accessibility. Using BPTF-null MEFs we show that BPTF is necessary for c-MYC-driven proliferation, G1-S progression, and replication stress, but not for c-MYC-driven apoptosis. Consistently, BPTF is required for the proliferation of cells driven by c-MYC, such as Burkitt lymphoma, and its expression in human cancer lines correlates with the activation of c-MYC gene signatures. Our findings point to the c-MYC-BPTF axis as a potential therapeutic target in cancer. To assess whether BPTF is required for the transcriptional activity of c-MYC, human foreskin fibroblasts (HFF) were stably transduced with the chimeric MYC-ER cDNA (HFF MYC-ER) and infected with lentiviruses coding for either control (shNt) or BPTF-targeting shRNAs. Cells were serum-starved for 2 days to achieve quiescence and then treated with 4-hydroxytamoxifen (4-OHT)

2016-01-19 | E-GEOD-65545 | biostudies-arrayexpress

BPTF is required for c-MYC-induced remodelling of target chromatin and transcriptional activation [ChIP-Seq]

2016-01-19 | E-GEOD-65544 | biostudies-arrayexpress