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MicroRNA expression in mouse oviduct and Dicer1 tumors

ABSTRACT: microRNA expression in mouse oviduct and Dicer1 tumors

PROVIDER: PRJNA976207 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24735479.fastq.gz	Fastqsanger.gz
	SRR24735480.fastq.gz	Fastqsanger.gz
	SRR24735481.fastq.gz	Fastqsanger.gz
	SRR24735482.fastq.gz	Fastqsanger.gz
	SRR24735483.fastq.gz	Fastqsanger.gz

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microRNA expression in mouse oviduct and Dicer1 tumors

Project description:We developed a genetically engineered conditional compound heterozygous Dicer1 mouse strain that fully recapitulates the bi-allelic mutations of DICER1 in DICER1 syndrome-associated cancers. Embryonic activation of bi-allelic Dicer1 mutations, driven by the anti-Müllerian hormone receptor 2 (Amhr2)-driven Cre strain (Amhr2+/cre), drove cancer development from oviduct. Small RNA sequencing was performed to compare the microRNA expression profiles between tumor and normal oviduct.

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Expression in mouse oviduct and Dicer1 tumors

Project description:Expression in mouse oviduct and Dicer1 tumors

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mRNA expression in mouse oviduct and Dicer1 tumors

Project description:We developed a genetically engineered conditional compound heterozygous Dicer1 mouse strain that fully recapitulates the bi-allelic mutations of DICER1 in DICER1 syndrome-associated cancers. Embryonic activation of bi-allelic Dicer1 mutations, driven by the anti-Müllerian hormone receptor 2 (Amhr2)-driven Cre strain (Amhr2+/cre), drove cancer development from oviduct. mRNA sequencing was performed to compare the mRNA expression profiles between tumor and normal oviduct.

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mRNA expression in mouse oviduct and Dicer1 tumors

Project description:mRNA expression in mouse oviduct and Dicer1 tumors

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Somatic mutations in DROSHA and DICER1 impair microRNA biogenesis in Wilms tumors

Project description:Through whole-exome sequencing we identified somatic missense mutations in DICER1 and DROSHA in Wilms tumor, a childhood kidney cancer. DICER1 and DROSHA are key enzymes in the microRNA biogenesis pathway. To determine the effect of these mutations on microRNA expression, we prepared small RNAs from Wilms tumors and used next-generation sequencing to determine the expression levels of microRNAs in the tumors. Comparison of miRNA expression in tumors with and without mutations in DICER1 or DROSHA.

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Somatic mutations in DROSHA and DICER1 impair microRNA biogenesis in Wilms tumors

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Project description:Mutations in the microRNA processing genes DICER1 and DROSHA drive childhood cancers such as pineoblastoma, a brain tumor that resembles undifferentiated precursors of the pineal gland. To understand how microRNAs regulate proliferation of these progenitors, we developed a mouse model of pineoblastoma by ablating Drosha or Dicer1 in the developing pineal gland. The tumors that arise in these models resemble proliferative, undifferentiated embryonic progenitors. They are marked by loss of microRNAs, including the let-7 family, and de-repression of let-7 target genes. One upregulated let-7 target gene is the oncofetal transcription factor Plagl2, which activates expression of key pro-growth genes Igf2 and Ccnd2, and we show that small molecules targeting these two drivers block tumor growth. Thus, our results demonstrate that tumors driven by loss of microRNA processing may be therapeutically targeted by inhibiting downstream drivers of proliferation.

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microRNA expression profile of MRC5-CAFs transfected with control siRNA (si-Ctrl) or Dicer1 specific siRNA (si-Dicer1) for 72 hr

Project description:Ovarian cancer (OC) remains the leading cause of death in patients with gynecological malignancy. An improved understanding of the genomics has led to the separation of OC into histologically and molecularly defined subgroups. Based on molecular profiling in OC patients, subtype with a reactivated tumor stroma presented the worst prognosis, emphasizing the importance of tumor microenvironment especially stromal fibroblasts in fueling OC progression. Dicer1 is well recognized as the microRNA (miR) synthesis machinery, playing a crucial role in cellular maturation and development, and was generally considered to be a tumor suppressor gene that inhibited tumor initiation and metastasis. Dicer1 expression pattern and exact biological function was seldom studied in the stromal compartment. There was a recent study demonstrating that Dicer1 was involved in mouse embryonic fibroblast (MEF) development and maturation. Therefore, we are inspired to explore the expression and function of Dicer1 in stromal fibroblasts of OC patients. In this study, mRNA and microRNA gene expression profiling were conducted for MRC5-CAFs after silencing of Dicer1. By comparing the expression data of MRC5-CAFs transfected with control siRNA (si-Ctrl) or with Dicer1 specific siRNA (si-Dicer1) for 72 hr, we identified a set of differential expressed mRNA and microRNA in MRC5-CAFs after Dicer1 knockdown. This study was the first to investigate Dicer1 influence of stromal fibroblast gene expression and the underlying regulation mechanism, which held great importance in complementing our understanding of Dicer1 in OC initiation and development, and raises potent therapeutical targets in controlling OC metastasis We used microarrays to profile the microRNA expression of MRC5-CAFs before and after Dicer1 knockdown, in order to identify microRNA alteration exerted by Dicer1 in the context of stromal fibroblasts.

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