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ChIP-Seq, CPD-Seq and RNA-Seq in retinoblastoma 1 (RB1) knock out cells

ABSTRACT: ChIP-Seq, CPD-Seq and RNA-Seq in retinoblastoma 1 (RB1) knock out cells

PROVIDER: PRJNA723856 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14301918_1.fastq.gz	Fastqsanger.gz
	SRR14301918_2.fastq.gz	Fastqsanger.gz
	SRR14301919_1.fastq.gz	Fastqsanger.gz
	SRR14301919_2.fastq.gz	Fastqsanger.gz
	SRR14301920_1.fastq.gz	Fastqsanger.gz

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

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Enhanced Innate Response In RB1 deficient Microglia Derived From Retinoblastoma Patient

Project description:Retinoblastoma (Rb), the most prevalent intraocular malignant tumor in children with global survival rate less than 30%, is mainly caused by the deficiency of the tumor suppressor RB1. A line of evidence have shown that local inflammation and immune escape play important roles in the occurrence of Rb, however the underlying mechanism remains unclear. We hypothesize that the unique neuroimmune cell type, retinal microglia, has a vital role in the Rb pathogenesis. In this study, we differentiated microglia cells (iMGs) from established induced pluripotent stem cells (iPSCs) derived from a retinoblastoma patient with the defined RB1 mutations. We investigated the function of RB1 in innate immune response of microglia and found that the expression of interleukins and chemokines, especially interleukin 6 and TNF-α, were highly upregulated in LPS-stimulated RB1 deficient iMGs, which enhanced innate immune responses and created a pro-inflammation environment. These findings demonstrated that RB1 is indispensable to maintain microglia function in innate immunity and its deficiency leads to enhanced inflammation responses, which may accelerate tumor growth and malignancy. This study provides new insights for pathological mechanism and immunotherapeutic target of retinoblastoma.

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