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Exploring the mechanism of transcription factor TAF7 promoting the progression of triple-negative breast cancer

ABSTRACT: Exploring the mechanism of transcription factor TAF7 promoting the progression of triple-negative breast cancer

PROVIDER: PRJNA1154263 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30541678_1.fastq.gz	Fastqsanger.gz
	SRR30541678_2.fastq.gz	Fastqsanger.gz
	SRR30541679_1.fastq.gz	Fastqsanger.gz
	SRR30541679_2.fastq.gz	Fastqsanger.gz
	SRR30541680_1.fastq.gz	Fastqsanger.gz

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Exploring the mechanism of transcription factor TAF7 promoting the progression of triple-negative breast cancer

Project description:To further study the regulation of TAF7 on cells, the transcriptome sequencing on MDA MB-231 cells, MDA MB-231/shTAF7 cells, MDA 231-LM2 and MDA 231-LM2/shTAF7 cells were performed.

2025-01-20 | GSE276005 | GEO

anti-TAF7 RIP-Seq identifies RNA species bound by cytoplasmic TAF7 in HeLa TAF7 (WT) cells

Project description:We perform TAF7 RIP-Seq to generate a transcriptome-view of RNA targets bound by TAF7

2021-10-22 | GSE161670 | GEO

Exploring mechanism the transcription factor SIPA1 promote the progression of triple-negative breast cancer

Project description:Exploring mechanism the transcription factor SIPA1 promote the progression of triple-negative breast cancer

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anti-TAF7 RIP-Seq identifies RNA species bound by cytoplasmic TAF7 in HeLa TAF7 (WT) cells

Project description:anti-TAF7 RIP-Seq identifies RNA species bound by cytoplasmic TAF7 in HeLa TAF7 (WT) cells

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FLAG RIP-Seq identifies RNA species bound by cytoplasmic TAF7 in HeLa TAF7 (WT) cells

Project description:We perform FLAG RIP-Seq to generate a transcriptome-view of RNA targets bound by TAF7

2021-10-22 | GSE161667 | GEO

Transcriptome profiling of HeLa TAF7 (WT) cytoplasmic extracts

Project description:We perform RNA-Seq to analyze gene expression profiles in HeLa TAF7 (WT) cytoplasmic extracts, which are the inputs of RIP-Seq and PAR-CLIP.

2021-10-22 | GSE161668 | GEO

Flt3L therapy induces a Treg‐promoting cDC1 state in triple‐negative breast cancer

Project description:Flt3L therapy induces a Treg‐promoting cDC1 state in triple‐negative breast cancer

| PRJNA936137 | ENA

The General Transcription Factor TAF7 is Essential for Embryonic Development but Not Essential for the Survival or Differentiation of Mature T Cells (MEF data)

Project description:TAF7, a component of the TFIID complex that nucleates the assembly of transcription preinitiation complexes, also independently interacts with and regulates the enzymatic activities of other transcription factors, including P-TEFb, TFIIH and CIITA, ensuring an orderly progression in transcription initiation. Since not all TAFs are required in terminally differentiated cells, we examined the essentiality of TAF7 in cells at different developmental stages in vivo. Germ-line disruption of the TAF7 gene is embryonic lethal between 3.5 and 5.5 days post coitus. TAF7-deleted mouse embryonic fibroblasts (MEFs) globally cease transcription and stop proliferating. In contrast, whereas TAF7 is essential for the differentiation and proliferation of immature thymocytes, it is not required for subsequent, proliferation-independent differentiation of lineage committed thymocytes or their egress into the periphery. TAF7 deletion in peripheral CD4+ T cells affects only a small number of transcripts. However, TAF7-deleted T cells are not able to undergo activation and expansion in response to antigenic stimuli. These findings suggest that TAF7 is essential for proliferation but not for proliferation-independent differentiation.

2012-04-01 | GSE34793 | GEO

The General Transcription Factor TAF7 is Essential for Embryonic Development but Not Essential for the Survival or Differentiation of Mature T Cells (T cell data)

2012-04-01 | GSE34795 | GEO

Flt3L therapy induces a Treg‐promoting cDC1 state in triple‐negative breast cancer

Project description:Conventional dendritic cells (cDCs) are at the forefront of activating the immune system to mount an anti‐tumor immune response. Flt3L is a cytokine required for DC development that can increase DC abundance in the tumor when administered therapeutically. However, the impact of Flt3L on the phenotype of distinct cDC subsets in the tumor microenvironment is still largely undetermined. Here, using multi‐omic single‐cell analysis, we show that Flt3L therapy increases all cDC subsets in orthotopic E0771 triple‐negative breast cancer, but this did not result in a reduction of tumor growth. Interestingly, a CD81+migcDC1 population, likely developing from cDC1, was induced upon Flt3L treatment. This subset is characterized by the expression of both canonical cDC1 markers as well as migratory cDC activation and regulatory markers and displayed a higher Treg‐inducing potential compared to other migcDCs. To shift the cDC phenotype towards a T‐cell stimulatory phenotype, CD40 agonist therapy was administered in combination with Flt3L. However, while αCD40 reduced tumor growth, Flt3L failed to improve the therapeutic response to αCD40 therapy. Interestingly, Flt3L+αCD40 combination therapy increased the abundance of Treg promoting CD81+migcDC1. Nonetheless, while Treg‐depletion and αCD40 therapy were synergistic, the addition of Flt3L to this combination did not result in any added benefit. Overall, these results indicate that merely increasing cDCs in the tumor by Flt3L treatment cannot improve anti‐tumor responses and therefore might not be beneficial for the treatment of triple‐negative breast cancer, though could still be of use to increase cDC numbers for autologous DC‐therapy.

2023-07-26 | GSE225539 | GEO

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