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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE200183 | GEO | 2023/12/13

REPOSITORIES: GEO

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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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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.

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

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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]

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CircRHOT1 restricts gastric cancer cell ferroptosis by epigenetically regulating GPX4

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Podofilox suppresses gastric cancer cell proliferation by regulating cell cycle arrest and the c-Myc/ATG10 axis.

Project description:Gastric cancer (GC) is a malignancy for which effective therapeutic drugs are limited. Podofilox exhibits antitumor effects in various types of cancer; however, whether it may inhibit GC growth remains unknown. The aim of the present study was to investigate the role of podofilox in GC. Cell Counting Kit-8, colony formation and cell cycle assays were used to detect the role of podofilox on cellular proliferation and the cell cycle, respectively. A microarray was used to detect the transcriptional changes induced by podofilox in GC cells. The results of the present study demonstrated that podofilox inhibited GC cell proliferation and colony formation. The half maximal inhibitory concentration of podofilox in AGS and HGC-27 cells was 2.327 and 1.981 nM, respectively. In addition, treatment with podofilox induced G0/G1 cell cycle arrest. Molecular analysis based on microarray data demonstrated that podofilox altered the expression levels of genes involved in the cell cycle, c-Myc and p53 signaling. Autophagy-related 10 (ATG10), which was highly expressed in GC tissues, was also downregulated by podofilox, as demonstrated by the results of the microarray analysis and immunoblotting. To determine the involvement of ATG10 in GC, ATG10 was knocked down in GC cells by small interfering RNA, which suppressed the proliferation and colony formation of GC cells compared with those observed in the control-transfected cells. Taken together, the results of the present study suggested that podofilox may inhibit GC cell proliferation by preventing the cell cycle progression and regulating the c-Myc/ATG10 signaling pathway.

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Histone demethylase KDM4C controls tumorigenesis of glioblastoma by epigenetically regulating p53 and c-Myc.

Project description:Glioblastoma is the most lethal brain tumor and its pathogenesis remains incompletely understood. KDM4C is a histone H3K9 demethylase that contributes to epigenetic regulation of both oncogene and tumor suppressor genes and is often overexpressed in human tumors, including glioblastoma. However, KDM4C's roles in glioblastoma and the underlying molecular mechanisms remain unclear. Here, we show that KDM4C knockdown significantly represses proliferation and tumorigenesis of glioblastoma cells in vitro and in vivo that are rescued by overexpressing wild-type KDM4C but not a catalytic dead mutant. KDM4C protein expression is upregulated in glioblastoma, and its expression correlates with c-Myc expression. KDM4C also binds to the c-Myc promoter and induces c-Myc expression. Importantly, KDM4C suppresses the pro-apoptotic functions of p53 by demethylating p53K372me1, which is pivotal for the stability of chromatin-bound p53. Conversely, depletion or inhibition of KDM4C promotes p53 target gene expression and induces apoptosis in glioblastoma. KDM4C may serve as an oncogene through the dual functions of inactivation of p53 and activation of c-Myc in glioblastoma. Our study demonstrates KDM4C inhibition as a promising therapeutic strategy for targeting glioblastoma.

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Long non-coding RNA NEAT1 increases the aggressiveness of gastric cancer by regulating the microRNA-142-5p/JAG1 axis.

Project description:Gastric cancer has been indicated to have a high recurrence rate in China. Previous studies have revealed that long non-coding RNA nuclear-enriched abundant transcript 1 (NEAT1) exerted critical roles in cancers. Therefore, the present study aimed to determine the function of NEAT1 and explore the unknown molecular mechanisms of gastric cancer pathogenesis. Reverse transcription-quantitative PCR assay was used to examine the expression of NEAT1, microRNA (miR)-142-5p and jagged1 (JAG1) in gastric cancer. Cell Counting Kit-8 and Transwell assays were conducted to examine cell proliferation, migration and invasion. The protein expression levels of N-cadherin, Vimentin, E-cadherin and JAG1 were quantified by western blot assay. The associations among NEAT1, miR-142-5p and JAG1 were confirmed by dual-luciferase reporter assay and RNA immunoprecipitation. The effects of NEAT1 silencing on tumor growth were evaluated by tumor xenografts. The results indicated that NEAT1 was highly expressed in tumor tissues and cells compared with that in paracancerous tissues and the normal gastric epithelial cell line GES-1 and significantly associated with poor prognosis in gastric cancer. Functional analyses further demonstrated that NEAT1 knockdown suppressed proliferation, motility and tumor growth in vitro and in vivo. Mechanistically, NEAT1 sponged miR-142-5p to regulate JAG1 expression. In addition, the effects of NEAT1 knockdown on the proliferation, migration and invasion of gastric cancer cells could be rescued by miR-142-5p inhibitor, and JAG1 overexpression reversed the miR-142-5p-mediated effects on gastric cancer cells. These findings demonstrated that long non-coding RNA NEAT1 regulated gastric cancer progression by targeting the miR-142-5p/JAG1 axis.

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