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Small RNA-sequencing of primary fibrolamellar carcinoma (FLC), FLC patient-derived xenograft, and maturational liver lineage stages

ABSTRACT: Fibrolamellar carcinoma (FLC) is a rare liver cancer. Here we characterized the small RNA expression landscape of primary FLC, a FLC patient-derived xenograft model, and normal maturational liver lineage stages

ORGANISM(S): Homo sapiens

PROVIDER: GSE114974 | GEO | 2019/03/07

REPOSITORIES: GEO

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Small RNA-sequencing of primary fibrolamellar carcinoma (FLC), FLC patient-derived xenograft, and maturational liver lineage stages

Project description:Small RNA-sequencing of primary fibrolamellar carcinoma (FLC), FLC patient-derived xenograft, and maturational liver lineage stages

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RNA-sequencing of fibrolamellar carcinoma (FLC) cell line treated with miR-375 mimic

Project description:Fibrolamellar carcinoma (FLC) is a rare liver cancer. Expression of miR-375 is significantly lost in primary FLC tumors compared to non-malignant liver. Here, we treated a FLC cell line with miR-375 mimic or scramble control to determine the function of miR-375 in FLC.

2019-03-07 | GSE125602 | GEO

RNA-sequencing analysis of human fibrolamellar hepatocellular carcinoma and 4 maturational stages of the human hepatobiliary system

Project description:The etiology of fibrolamellar hepatocellular carcinoma (FL-HCC), a liver cancer occurring increasingly in children to young adults, is poorly understood. We performed high-throughput sequencing on mRNA isolated from a newly developed model of FL-HCC and 4 different maturational lineages of the hepatobiliary system. Our results indicate that the transcriptome of FL-HCC is most similar to that of biliary tree stem cells.

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Transcription profiling by array of Pure Fibrolamellar Hepatocellular carcinoma

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

Chromatin run-on and RNA sequencing of fibrolamellar carcinoma

Project description:Fibrolamellar carcinoma (FLC) is a rare, therapeutically intractable liver cancer that disproportionately affects youth. Here we used chromatin run-on sequencing to characterize the enhancer landscape in FLC and RNA sequencing to identify dysregulated genes in FLC.

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Chemical, molecular, and single cell analysis reveal chondroitin sulfate proteoglycan aberrancy in fibrolamellar carcinoma

Project description:Fibrolamellar carcinoma (FLC) is an aggressive liver cancer that predominantly afflicts adolescents and young adults. Patients with FLC are characterized by a heterozygous deletion on chromosome 19 that creates an oncogenic gene fusion, DNAJB1-PRKACA. The extracellular environment of FLC tumors is poorly characterized and may contribute to cancer progression, metastasis, and/or drug resistance. To bridge this knowledge gap, we propose to assess pathways relevant to proteoglycans, a major component of the extracellular matrix. We leveraged single-cell ATAC-seq to analyze the diversity of VCAN accessibility across different cell types.

2022-05-20 | GSE202315 | GEO

GENOMIC ANALYSIS OF FIBROLAMELLAR HEPATOCELLULAR CARCINOMA REVEALS A UNIQUE MOLECULAR PROFILE

Project description:Fibrolamellar hepatocellular carcinoma (FLC) is a rare primary hepatic cancer usually developed in non-cirrhotic livers of children and young adults with unknown etiology. Treatment is limited to surgical intervention. To date, molecular pathogenesis of FLC has been poorly characterized. A cohort of FLCs was analyzed through SNP-array. GISTIC algorithm identified chromosomal aberrations. FLC tumors corresponding to 25 different patients. In all cases, tumor and corresponding non-tumor samples were frozen (-80°C) after hepatic resection at diagnosis. Comparative Genomic Hybridization analysis was done using Illumina HumanHap370CNV Genotyping BeadChip SNP array

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Retinoic acid treatment suppresses fibrolamellar carcinoma growth

Project description:Fibrolamellar carcinoma (FLC) is a devastating, early-onset rare cancer for which there is no effective standard of care. FLC tumors are initiated and likely also maintained by the fusion oncoprotein DNAJ-PKAc (DP). Strategies to therapeutically target DP are underway but remain challenging. Alternate therapeutic approaches are needed in order to maximize the potential benefit for patients. In this study, to identify candidate compounds for drug repurposing, we re-analyzed publicly available RNA-seq data in FLC and non-malignant liver (NML) tissue. We noted that retinoid metabolism, a normal function of a healthy liver, is strikingly suppressed in FLC, which led to the hypothesis that FLC tumors may be responsive to all-trans retinoic acid (ATRA). To test this hypothesis, we treated FLC tumor cells in culture, established from a patient-derived xenograft (PDX) mouse model, with ATRA and found by RNA-seq that well-established molecular markers of PKA signaling and FLC tumors are significantly reduced. Moreover, ATRA treatment markedly diminished cell viability, proliferation, and colony forming capability. We also demonstrated that ATRA sensitizes FLC cells to apoptotic induction by the TLR3 ligand, poly(I:C). Next, using patient tissue slices, we confirmed that ATRA reduces cell viability only in tumors and not in adjacent NML tissue. Finally, we performed in vivo studies in PDX mice to show that ATRA significantly suppresses FLC tumor growth. These findings motivate a more expansive pre-clinical examination of ATRA, especially in conjunction with TLR3 ligands and possibly other adjuvants, to establish the safety and efficacy of ATRA for FLC clinical trials.

2023-02-13 | GSE224888 | GEO

Centrosomal Localization of DNAJ-PKAc Fusion Heightens PLK1 Inhibitor Sensitivity in Fibrolamellar Cancer

Project description:Fibrolamellar carcinoma (FLC), a rare and fatal liver cancer lacking effective drug therapy, is driven by the DNAJ-PKAc fusion oncoprotein. However, the underlying mechanism of DNAJ-PKAc's role in FLC tumor growth remains enigmatic. Employing an unbiased systems-based approach, we uncovered a new role of DNAJ-PKAc oncoprotein in FLC and identified downstream kinases involved in this process. Functional screening, coupled with computational analysis, highlighted Polo-like kinase 1 (PLK1) as vital for FLC cell viability. Genetic and pharmacological PLK1 inhibition significantly reduced FLC cell growth, inducing apoptosis. Further studies showed DNAJ-PKAc's centrosomal presence and direct interaction with PLK1, revealing a novel mechanism that promotes PLK1 activation and mitotic progression. Clinical-grade PLK1 inhibitors effectively suppressed FLC tumor growth across multiple preclinical models, including patient-derived xenograft and an orthotopic model of FLC, suggesting promising therapeutic avenues. Our findings underscore the role of DNAJ-PKAc in rewiring signaling networks and highlight valuable clinical implications for PLK1-targeted therapies for FLC.

2023-12-19 | GSE250059 | GEO

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

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