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Genome-wide identification of AP-2α targets in bladder cells by RNA-seq

ABSTRACT: Genome-wide identification of AP-2α targets in bladder cells by RNA-seq

PROVIDER: PRJNA528625 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8769761.fastq.gz	Fastqsanger.gz
	SRR8769762.fastq.gz	Fastqsanger.gz
	SRR8769763.fastq.gz	Fastqsanger.gz
	SRR8769764.fastq.gz	Fastqsanger.gz
	SRR8769765.fastq.gz	Fastqsanger.gz

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Genome-wide identification of AP-2α targets in bladder cells by RNA-seq (Control vs AP-2α KD)

Project description:Genome-wide identification of AP-2α targets in bladder cells by RNA-seq (Control vs AP-2α KD)

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Genome-wide identification of AP-2α targets in bladder cells by RNA-seq (Control vs AP-2α OE)

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Genome-wide identification of AP-2α targets in bladder cells by RNA-seq (Control vs AP-2α OE)

Project description:TFAP2A (AP-2α) is a member of the transcription factor AP-2 family, functions as a tumor suppressor by regulating the expression of various cancer-related genes; its expression is positively correlated with chemosensitivity and survival of cancer patients.

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Genome-wide identification of AP-2α targets in bladder cells by RNA-seq (Control vs AP-2α KD)

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Determination of the WWOX gene function in modulating cellular pathways activated by AP-2α and AP-2γ transcription factors in bladder cancer

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AP-2α Regulates S-phase and is a Marker for Sensitivity to PI3K-inhibitor Buparlisib in Colon Cancer [ChIP-seq]

Project description:Abstract:AP-2α (encoded by TFAP2A) functions as a tumor suppressor and influences response to therapy in several cancer types. We aimed to characterize regulation of the transcriptome by AP-2α in colon cancer. Results: Knockout of TFAP2A induced significant alterations in the transcriptome including repression of TGM2, identified as a primary gene target of AP-2α. Loss of AP-2α delayed progression through S-phase into G2/M and decreased phosphorylation of AKT, effects that were mediated through regulation of TGM2. Buparlisib (BKM120) repressed in vitro invasiveness of HCT116 and LS-180; however, loss of AP-2α induced resistance to Buparlisib. Similarly, Buparlisib repressed PHH3 and growth of tumor xenografts and increased overall survival of tumor-bearing mice, whereas, loss of AP-2α induced resistance to the effect of PI3K inhibition. Conclusion: Loss of AP-2α in colon cancer leads to prolonged S-phase through altered activation of AKT leading to resistance to the PI3K inhibitor, Buparlisib. The findings demonstrate an important role for AP-2α in regulating progression through the cell cycle and indicates that AP-2α is a marker for response to PI3K inhibitors.

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AP-2α Regulates S-phase and is a Marker for Sensitivity to PI3K-inhibitor Buparlisib in Colon Cancer [RNA-seq]

2021-06-01 | GSE155162 | GEO

Genome-wide identification of AP-2α targets in bladder cells by RNA-seq

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

2020-12-08 | GSE128716 | GEO