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Sall4 guides p53-mediated enhancer interference upon DNA damage in mouse embryonic stem cells

ABSTRACT: Sall4 guides p53-mediated enhancer interference upon DNA damage in mouse embryonic stem cells

PROVIDER: PRJNA828416 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18829226_1.fastq.gz	Fastqsanger.gz
	SRR18829226_2.fastq.gz	Fastqsanger.gz
	SRR18829227_1.fastq.gz	Fastqsanger.gz
	SRR18829227_2.fastq.gz	Fastqsanger.gz
	SRR18829231_1.fastq.gz	Fastqsanger.gz

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Sall4 guides p53-mediated enhancer interference upon DNA damage in mouse embryonic stem cells

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p53-dependent regulation of gene expression following DNA damage

Project description:Long noncoding RNAs (lncRNAs) are prevalent genes with frequently exquisite regulation but mostly unknown functions. Here we demonstrate a role of lncRNAs in guiding signal transduction. DNA damage activates transcription of DINO (Damage Induced NOncoding) via p53. DINO knockdown blocks DNA damage-induced gene expression and cell cycle arrest. Conversely, enforced expression of DINO activates damage signaling without DNA damage. DINO binds p53 and selectively promotes SET7 methylation of p53 at lysine 372 over other substrates, which stabilizes p53 in an auto-amplification loop. Our results suggest that inducible lncRNA can achieve catalysis-like effects to rewire cellular signaling networks. RNA was isolated from human fetal lung fibroblasts, HCT116 p53+/+, or HCT116 p53-/- cells treated with doxorubicin or sham for 26 hours. Human fetal lung fibroblasts were transfected with siRNAs targeting DINO or non-targeting control and subsequently treated with doxorubicin for 26 hours.

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Targeting the novel SALL4/CBL-B pathway by HDAC inhibitor MS-275 in lung cancer

Project description:The overall survival of lung cancer patients remains dismal despite the availability of targeted therapies. Oncofetal protein SALL4 is a novel cancer target. We herein report that SALL4 was aberrantly expressed in a subset of lung cancer patients with poor survival. SALL4 silencing by RNA interference or SALL4 peptide inhibitor treatment led to impaired lung cancer cell growth. Expression profiling on SALL4-knockdown cells demonstrated that both the EGFR and IGF1R signaling pathways were affected. Further studies revealed that SALL4 suppresses these pathways indirectly by repressing CBL-B. Connectivity Map analysis revealed HDAC inhibitor MS-275 as a potential drug in treating SALL4-expressing cancers and this was confirmed using 17 lung cancer cell lines. In summary, we report for the first time that MS-275 can target the novel SALL4/CBL-B pathway in lung cancer. This lays the foundation for future clinical studies to evaluate the therapeutic efficacy of MS-275 in SALL4-positive lung cancer patients.

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