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

ABSTRACT: AP-2α Regulates S-phase and is a Marker for Sensitivity to PI3K-inhibitor Buparlisib in Colon Cancer

PROVIDER: PRJNA648910 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12329900_1.fastq.gz	Fastqsanger.gz
	SRR12329900_2.fastq.gz	Fastqsanger.gz
	SRR12329901_1.fastq.gz	Fastqsanger.gz
	SRR12329901_2.fastq.gz	Fastqsanger.gz
	SRR12329902_1.fastq.gz	Fastqsanger.gz

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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 [ChIP-seq]

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

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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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