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Multi-omic analysis of microRNA-mediated regulation reveals a proliferative axis involving miR-10b in fibrolamellar carcinoma

ABSTRACT: Multi-omic analysis of microRNA-mediated regulation reveals a proliferative axis involving miR-10b in fibrolamellar carcinoma

PROVIDER: PRJNA753872 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15417902.fastq.gz	Fastqsanger.gz
	SRR15417903.fastq.gz	Fastqsanger.gz
	SRR15417904.fastq.gz	Fastqsanger.gz
	SRR15417905.fastq.gz	Fastqsanger.gz
	SRR15417906.fastq.gz	Fastqsanger.gz

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Multi-omic analysis of microRNA-mediated regulation reveals a proliferative axis involving miR-10b in fibrolamellar carcinoma

Project description:Fibrolamellar carcinoma (FLC) is an aggressive liver cancer with low survival rates and no standard-of-care. The vast majority of FLC patients carry a causative somatic mutation that leads to the gene fusion, DNAJB1-PRKACA. To work toward novel therapeutic strategies, it is important to understand the mechanisms underlying FLC etiology and progression. To that end, in this study, we analyzed a large sample cohort (52 patients) using multiple genome-scale assays to define genes subject primarily to post-transcriptional regulation by microRNAs. These studies revealed a candidate master microRNA regulator in FLC, miR-10b. Functional experiments in cells established from a patient-derived xenograft model revealed that miR-10b contributes to FLC cell metabolic health and proliferation.

2021-11-03 | GSE181922 | GEO

Multiomic analysis of microRNA-mediated regulation reveals a proliferative axis involving miR-10b in fibrolamellar carcinoma.

Project description:Fibrolamellar carcinoma (FLC) is an aggressive liver cancer primarily afflicting adolescents and young adults. Most patients with FLC harbor a heterozygous deletion on chromosome 19 that leads to the oncogenic gene fusion, DNAJB1-PRKACA. There are currently no effective therapeutics for FLC. To address that, it is critical to gain deeper mechanistic insight into FLC pathogenesis. We assembled a large sample set of FLC and nonmalignant liver tissue (n = 52) and performed integrative multiomic analysis. Specifically, we carried out small RNA sequencing to define altered microRNA expression patterns in tumor samples and then coupled this analysis with RNA sequencing and chromatin run-on sequencing data to identify candidate master microRNA regulators of gene expression in FLC. We also evaluated the relationship between DNAJB1-PRKACA and microRNAs of interest in several human and mouse cell models. Finally, we performed loss-of-function experiments for a specific microRNA in cells established from a patient-derived xenograft (PDX) model. We identified miR-10b-5p as the top candidate pro-proliferative microRNA in FLC. In multiple human cell models, overexpression of DNAJB1-PRKACA led to significant upregulation of miR-10b-5p. Inhibition of miR-10b in PDX-derived cells increased the expression of several potentially novel target genes, concomitant with a significant reduction in metabolic activity, proliferation, and anchorage-independent growth. This study highlights a potentially novel proliferative axis in FLC and provides a rich resource for further investigation of FLC etiology.

| S-EPMC9220943 | biostudies-literature

Transcription profiling by array of Pure Fibrolamellar Hepatocellular carcinoma

Project description:A Cartes d'Identite des Tumeurs (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net) | Affymetrix HG-U133 Plus 2.0 : 5 mixed fibrolamellar carcinoma (m-FLC), 17 pure fibrolamellar carcinoma (p-FLC), 7 hepatocelluar carcinoma arising in non-cirrhotic liver (nc-HCC) and 10 non-tumoral livers (NL).

2014-08-15 | E-MTAB-1503 | biostudies-arrayexpress

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Project description:miR-10b precusor or miR-10b inhibitor was used to overexpress or knockdown miR-10b expression in PANC-1 cells. Microarray analysis was used to characterize the changes in gene expression profiles of PANC-1 upon miR-10b overexpression or knockdown

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Acidothermus cellulolyticus strain:10B

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Salinibacter sp. 10B

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Project description:Background/ Aim: Diabetes has substantive co-occurrence with disorders of gut-brain interactions (DGBIs). The pathophysiological and molecular mechanisms linking diabetes and DGBIs are unclear. miRNAs are key regulators of diabetes and gut dysmotility. We investigated whether impaired gut barrier function regulated by a key miRNA, miR-10b-5p, links diabetes and gut dysmotility. Methods: We created a new mouse line using the Mb3Cas12a/Mb3Cpf1 endonuclease to knock out mir-10b globally. Loss of function studies were conducted to characterize diabetes, gut dysmotility, and gut barrier dysfunction phenotypes in these mice. Gain of function studies were conducted by injecting these mice with a miR-10b-5p mimic. Further, we performed miRNA-sequencing analysis from colonic mucosa from mir-10b KO, WT, and miR-10b-5p mimic injected mice to confirm 1) deficiency of miR-10b-5p in KO mice, and 2) restoration of miR-10b-5p expression after the mimic injection. Results: Congenital loss of mir-10b in mice led to the development of hyperglycemia, gut dysmotility, and gut barrier dysfunction. We found increased gut permeability and reduced expression of the tight junction protein Zonula occludens-1 (ZO-1), in the colon of mir-10b KO mice. We further confirmed that patients with diabetes or IBS-C, a known DGBI that is linked to leaky gut, had significantly reduced miR-10b-5p expression. Injection of a miR-10b-5p mimic in mir-10b KO mice rescued these molecular alterations and phenotypes. Conclusion: Our study uncovered a potential pathophysiologic mechanism of gut barrier dysfunction that links both the diabetes and gut dysmotility phenotypes in mice lacking miR-10b-5p. Treatment with a miR-10b-5p mimic reversed the leaky gut, diabetic, and gut dysmotility phenotypes, highlighting the translational potential of miR-10b-5p mimic.

2023-07-13 | GSE236981 | GEO

Bradyrhizobium sp. 8-10B

Project description:Bradyrhizobium sp. 8-10B Genome sequencing

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Multi-omic dissection of oncogenically active epiproteomes identifies drivers of proliferative or invasive breast tumors

Project description:Here we present a functional multi-omics method, interaction-Correlated Multi-omic Aberration Patterning or iC-MAP, which dissects intra-tumor heterogeneity and identifies in situ in real time the oncogenic consequences of multi-omics aberrations that drive proliferative/invasive tumor in individuals with poor prognosis. First, given epigenetic aberrations resulting from complex interactions between genetic susceptibility and environmental influences are the primary driving force of tumorigenesis, we applied our chromatin activity-based chemoproteomics (ChaC) method to characterize the tumor-phenotypic epiproteomes (epigenetic regulatory proteomes) in breast cancer (BC) patient tissues. A biotinylated ChaC probe UNC0965 that specifically binds to the oncogenically active histone methyltransferase G9a enabled the sorting/enrichment of a G9a-interacting epiproteome representing the predominant BC subtype in a tissue, which is separated from other cell types, especially non-malignant cells where G9a is less enzymatically active. ChaC then identified UNC0965-captured G9a interactors that are mostly involved in the oncogenic pathways associated with tumor cell viability and invasion. Using BC patient transcriptomic/genomic data we retrospectively identified the G9a interactor-encoding genes that show individualized iC-MAP in BC-subtypic patients with incurable metastatic disease, revealing essential drivers of proliferative or invasive BC phenotypes. Our iC-MAP findings can not only act as new diagnostic/prognostic markers to identify patient subsets with metastatic disease but also create precision therapeutic strategies that can match proliferative or invasive potential of individual patients.

2019-07-26 | PXD013795 | Pride

Genome profiling of fibrolamellar carcinoma [CGH]

Project description:Fibrolamellar hepatocellular carcinoma (FL-HCC) is a rare variant of HCC that most frequently affects young adults. Because of its rarity and an absence of preclinical models, the molecular biology of FL-HCC remains unclear. Our objective was to analyze chromosomal alterations and dysregulated gene expression in tumor specimens collected at a single center during two decades of experience with FL-HCC.

2017-06-09 | GSE64103 | GEO

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