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RNA sequencing analysis of wild-type and ITF2357 or I-BET151 or JQ1 treated mouse pancreatic cancer KPC cells

ABSTRACT: The ITF2357, I-BET151 and JQ1 promote antigen presentation and sensitize pancreatic cancer to T cell cytotoxicity, in combination with Immune checkpoint blockage therapy suppress tumor cell growth

ORGANISM(S): Mus musculus

PROVIDER: GSE216552 | GEO | 2025/10/25

REPOSITORIES: GEO

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Expression DATA from E11.5 pancreatic buds treated with I-BET151 or JQ1 for 24h

Project description:Bromodomain and Extra-terminal (BET) proteins are epigenetic readers that interact with acetylated lysines of histone tails. Recent studies have demonstrated their role in cancer progression, as they recruit key components of the transcriptional machinery to modulate gene expression. However, their role during embryonic development of the pancreas has never been studied. Using mouse embryonic pancreatic explants and human IPSC, we show that inhibition of BET proteins with either I-BET151 or JQ1 dramatically enhances the number of neurogenin3 (NEUROG3) endocrine progenitors, leading to an increased number of endocrine cells in the pancreatic explants. Despite inducing several β cell markers, BETi also strongly down-regulated Ins1 expression in developed explants and adult β cells. However, removal of BETi from explants prior to β cell development, as NEUROG3 expression peaks, further led to enhanced β cell development with higher expression of insulin and maturation markers UCN3 and MAFA. Altogether, these results show that BET proteins play a major role in the pancreas endocrine differentiation. Furthermore, they highlight the potential use of BETi to improve β cell replacement therapies.

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Expression DATA from E11.5 pancreatic buds treated with I-BET151 or JQ1 for 24h

Project description:Expression DATA from E11.5 pancreatic buds treated with I-BET151 or JQ1 for 24h

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RNA sequencing analysis of wild-type and ITF2357 or I-BET151 or JQ1 treated mouse pancreatic cancer KPC cells

Project description:RNA sequencing analysis of wild-type and ITF2357 or I-BET151 or JQ1 treated mouse pancreatic cancer KPC cells

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RNA-seq analysis of HNSCC cells after JQ1 treatment

Project description:We performed RNA sequencing (RNA-seq) of HNSCC cells to examine genome-wide gene expression pattern following JQ1 treatment. BET inhibition by JQ1 significantly inhibits a cohort of key oncogenes associate with tumorigenesis and metastasis. Suggesting BET inhibition is effective strategy to suppress the tumorigenesis and metastasis of head and neck squamous cell carcinoma.

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Thermal proteome profiling of JQ1

Project description:Goal of this experiment was the identification of proteins affected in their thermal stability by JQ1.

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BMDM treated with I-BET151 and sitmulated with IgG immune complex

Project description:Bone marrow derived macrophages were cultured and stimulated with I-BET151 or DMSO control, and stimulated with Ovalbumin-IgG immune complex or Ovalbumin control.

2022-05-02 | GSE200033 | GEO

BMDC treated with I-BET151 and sitmulated with IgG immune complex

Project description:Bone marrow derived dendritic cells were cultured and stimulated with I-BET151 or DMSO control, and stimulated with Ovalbumin-IgG immune complex or Ovalbumin control.

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2 Dimensional Thermal proteome profiling of JQ1

Project description:Goal of this experiment was the identification of proteins affected dose dependently in their thermal stability by JQ1.

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Multiplexed proteome dynamics profiling of JQ1-PROTAC

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ChIP-seq analysis of BRD4, MED1 and P65 in SCC1 cells after JQ1 treatment

Project description:To explore genome-wide alteration of BRD4, MED1, p65 and H3K27Ac during BET inhibition, we performed chromatin immunoprecipitation sequencing (ChIP-seq) of SCC1 cells to examine genome-wide recruitment of the MED1, BRD4, p65 and H3K27ac following JQ1 treatment. BET inhibition by JQ1 led to dramatically loss of the recruitment of MED1, BRD4 and p65 at a cohort of key oncogenes associate with tumorigenesis and metastasis. Suggesting BET inhibition is effective strategy to suppress the tumorigenesis and metastasis of head and neck squamous cell carcinoma.

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