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Phosphine-Nitrogen-Phosphine chelated CoCl2 (Co68) is a novel therapeutic agent for pancreatic cancer [ATAC-seq]

ABSTRACT: Phosphine-Nitrogen-Phosphine chelated CoCl2 (Co68) is a novel therapeutic agent for pancreatic cancer [ATAC-seq]

PROVIDER: PRJNA1218420 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32203170_1.fastq.gz	Fastqsanger.gz
	SRR32203170_2.fastq.gz	Fastqsanger.gz
	SRR32203171_1.fastq.gz	Fastqsanger.gz
	SRR32203171_2.fastq.gz	Fastqsanger.gz
	SRR32203172_1.fastq.gz	Fastqsanger.gz

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Phosphine-Nitrogen-Phosphine chelated CoCl2 (Co68) is a novel therapeutic agent for pancreatic cancer [RNA-seq]

Project description:Phosphine-Nitrogen-Phosphine chelated CoCl2 (Co68) is a novel therapeutic agent for pancreatic cancer [RNA-seq]

| PRJNA1218427 | ENA

Phosphine-Nitrogen-Phosphine chelated CoCl2 (Co68) is a novel therapeutic agent for pancreatic cancer [scRNA-seq]

Project description:Phosphine-Nitrogen-Phosphine chelated CoCl2 (Co68) is a novel therapeutic agent for pancreatic cancer [scRNA-seq]

| PRJNA1218426 | ENA

Phosphine-Nitrogen-Phosphine chelated CoCl2 (Co68) is a novel therapeutic agent for pancreatic cancer [scRNA-seq]

Project description:Pancreatic cancer is projected to become the second leading cause of cancer-related deaths globally by 2030, yet effective therapeutic options remain limited. Within the pancreatic cancer tumor microenvironment (TME), tumor-associated macrophages (TAMs) secrete interleukin-1 beta (IL-1β), promoting cancer progression while suppressing type I interferons (IFN-I), which is critical for effective tumor treatment. Utilizing the convolutional neural network (CNN)-based DLINP model developed in our laboratory, we identified Co68—an effective metal catalyst featuring a Phosphine-Nitrogen-Phosphine (PNP)-chelated CoCl₂ complex—as a promising candidate to modulate these immune pathways. In preclinical animal models, Co68 demonstrated superior antitumor efficacy compared to the STING agonist DMXAA and showed enhanced therapeutic effects when combined with PD-1 blockade. Single-cell RNA sequencing (scRNA-seq) revealed that Co68 reprograms TAMs to express interferon-stimulated genes (ISGs), attenuates pro-inflammatory cytokine secretion, and disrupts the IL-1β-PGE2 feedback loop, thereby facilitating the recruitment of NK and cytotoxic CD8+ T cells into the TME. Mechanistically, Co68 activates the IFN-I signaling pathway through the TLR4-TRIF-IFN-I axis and weakens inflammation via the TLR4-SYK-STAT1 pathway. Collectively, these findings highlight the therapeutic potential of Co68, derived from PNP-pincer chemistry, to reshape immune dynamics within the pancreatic cancer TME, positioning it as a promising candidate for innovative immunotherapy strategies.

2025-02-09 | GSE288555 | GEO

Phosphine-Nitrogen-Phosphine chelated CoCl2 (Co68) is a novel therapeutic agent for pancreatic cancer [RNA-seq]

2025-02-09 | GSE288554 | GEO

Phosphine-Nitrogen-Phosphine chelated CoCl2 (Co68) is a novel therapeutic agent for pancreatic cancer [ATAC-seq]

2025-02-09 | GSE288553 | GEO

Morusinol is a Potent Therapeutic Agent Against DLBCL

Project description:Morusinol is a Potent Therapeutic Agent Against DLBCL

| PRJNA956550 | ENA

Development of gene expression signatures for WT (Hif1afl/fl) mice and VSMC-specific HIF1α disruption (Hif1a△SMC) mice VSMCs treated with 150μM CoCl2 for 24hours

Project description:HIF1α is a key regulator of hypoxia, however, the changes of its target genes in VSMCs under hypoxia were unknown. CoCl2 is a chemical hypoxia agent which leads to the stabilization of HIF1-α and the expression of hypoxia responsive genes, Therefore Hif1afl/fl and Hif1a△SMC VSMCs were treated with CoCl2 and performed microarray analysis. We used microarray to detail the gene expression of WT (Hif1afl/fl) mice and VSMC-specific HIF1α disruption (Hif1a△SMC) mice VSMCs treated with 150μM CoCl2 for 24hours.

2020-06-22 | GSE119226 | GEO

CoCl2 induced cytotoxicity is associated with dysregulated lncRNAs expression

Project description:To investigate differentially expressed lncRNAs in C2C12 myotubes with/without CoCl2 treatment, we used mouse lncRNA microarray to examine the expression of lncRNAs in C2C12 myotubes and C2C12 myotubes with CoCl2 treatment.

2021-05-28 | GSE115089 | GEO

CoCl2 induced cytotoxicity is associated with dysregulated circRNAs expression

Project description:To investigate differentially expressed circRNAs in C2C12 myotubes with/without CoCl2 treatment, we used mouse circRNA microarray to examine the expression of circRNAs in C2C12 myotubes and C2C12 myotubes with CoCl2 treatment.

2021-05-28 | GSE115088 | GEO

CoCl2 Response in Cryptococcus neoformans

Project description:We investigated the effects of the hypoxia-mimetic CoCl2 on the gene expression of pathogenic fungus Cryptococcus neoformans. Keywords: compound treatment design

2009-05-01 | GSE11390 | GEO

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