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Genome-wide identification of transcripts associated with SNHG10 by ChIRP-seq

ABSTRACT: Understanding the roles of ncRNAs in tumorigenesis and metastasis would establish avenues for the identification of diagnostic and therapeutic targets. We observed that lncRNA SNHG10 and its derived SCARNA13 were concomitantly upregulated in hepatocellular carcinoma (HCC) pulmonary metastases and associated with poor prognosis. Mechanistically, SCARNA13, modulated by SNHG10, facilitated the cell cycle and epithelial-mesenchymal transition (EMT) of HCC cells by promoting SOX9. SNHG10 served as a sponge for miR-150-5p and interacted with RPL4 mRNA to increase the expression and activity of c-Myb. Reciprocally, upregulated and hyperactivated c-Myb enhanced SNHG10 and SCARNA13 expression through regulating SNHG10 promoter activity, forming a positive feedback loop and continuously stimulating SCARNA13 expression. Our findings characterized a complex epigenetic cause of HCC with clinical implications.

ORGANISM(S): Homo sapiens

PROVIDER: GSE119773 | GEO | 2018/09/12

REPOSITORIES: GEO

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Gene expression profiling of HCCLM3 cells: Control ASO vs SCARNA13 ASO

Project description:Understanding the roles of ncRNAs in tumorigenesis and metastasis would establish avenues for the identification of diagnostic and therapeutic targets. We observed that lncRNA SNHG10 and its derived SCARNA13 were concomitantly upregulated in hepatocellular carcinoma (HCC) pulmonary metastases and associated with poor prognosis. Mechanistically, SCARNA13, modulated by SNHG10, facilitated the cell cycle and epithelial-mesenchymal transition (EMT) of HCC cells by promoting SOX9. SNHG10 served as a sponge for miR-150-5p and interacted with RPL4 mRNA to increase the expression and activity of c-Myb. Reciprocally, upregulated and hyperactivated c-Myb enhanced SNHG10 and SCARNA13 expression through regulating SNHG10 promoter activity, forming a positive feedback loop and continuously stimulating SCARNA13 expression. Our findings characterized a complex epigenetic cause of HCC with clinical implications.

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Transcriptome of hepatocellular carcinoma using CAGE

Project description:An increasing number of non-coding RNAs (ncRNAs) are implicated in various human diseases including cancer; however ncRNA transcriptome of hepatocellular carcinoma (HCC) remains largely unexplored. We use CAGE (Cap Analysis of Gene Expression) to comprehensively map transcription start sites (TSSs) across different etiologies of human HCC as well as mouse HCC, with particular emphasis on ncRNAs distant from protein-coding genes. We find thousands of significantly up-regulated distal ncRNAs in HCC tumors compared to their matched non-tumors, which are as many as protein-coding genes. Moreover, we identify many LTR retroviral promoters activated in HCC tissues and expressed in a subfamily-specific manner, which account for approximately 20% of the up-regulated distal ncRNAs. The transcripts derived from LTRs, determined by 3' RACE, are multi-exon nuclear ncRNAs typically 0.5-2kb in length. This study sheds light on ncRNA transcriptome of human and mouse HCC. Expression profiles using CAGE for 37 mouse HCC. The human data are archived at dbGaP (phs000885.v1.p1). An umbrella BioProject has been created to associate the GEO and dbGaP BioProjects: PRJNA278792

2015-09-10 | E-GEOD-60982 | biostudies-arrayexpress

Transcriptome of hepatocellular carcinoma using CAGE

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Exosomal circRNA-MANBA mediates sorafenib resistance of hepatocellular carcinoma via miR-1290/CD109/p-STAT3 (Ser727) axis

Project description:Circular RNAs (circRNAs) are increasingly gaining importance and attention due to their diverse potential functions. Our study aims to explore the novel mechanisms by which exosome-contained circRNAs promote sorafenib resistance in hepatocellular carcinoma (HCC). Here we report that a circular RNA, circRNA-MANBA (a circular RNA upregulated in exosomes derived from sorafenib-resistant HCC cells), plays a significant role in sorafenib resistance in HCC. We identified that circRNA-MANBA is increased in sorafenib-resistant HCC cells, their exosomes, and tumor samples from sorafenib-treated HCC patients. Depletion of circRNA-MANBA substantially increases the cell-killing ability of sorafenib. Co-culture experiments revealed that exosomes from sorafenib-resistant HCC cells carrying large amounts of circRNA-MANBA could transmit drug resistant capacity to parental cells. Further studies revealed that circRNA-MANBA acted as ‘miRNAs sponge’ to absorb miR-1290, which prevented miR-1290 interaction with CD109 and thus upregulated STAT3 phosphorylation subsequently. Using different HCC mouse models, we demonstrated that silencing circRNA-MANBA by injection of siRNA could substantially overcome sorafenib resistance. Our study provides a proof-of-concept demonstration for a potential strategy to overcome sorafenib resistance in HCC patients by targeting circRNA-MANBA.

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cDCBLD2 mediates sorafenib resistance in hepatocellular carcinoma by sponging miR-345-5p binding to the TOP2A coding sequence

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A Mammalian Conserved Circular RNA CircLARP2 Regulates Hepatocellular Carcinoma Metastasis and Lipid Metabolism (Part 2)

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Project description:To explore the potential involvement of lncRNAs in hepatocellular carcinoma (HCC) oncogenesis, we conducted lncRNA and mRNA profiling in 3 pairs of human HCC and adjacent normal tissue (NT) by microarray. With abundant probes accounting for 33,045 lncRNAs and 30,215 coding transcripts in our microarray, the number of lncRNAs and coding transcripts that could be detected here is 10,149 and 14,944, respectively. From the data, thousands of lncRNAs and mRNAs were found to bedifferentially expressed (Fold Change≥2.0) in HCC tissues compared with NT and identified 624 lncRNAs and 1050 mRNAs were differentially expressed in all three HCC tissues.Bioinformatic analysis (gene ontology, pathway and network analysis) was performed for further study of these differentially expressed mRNAs.By qRT-PCR analysis in nineteen pairs HCC and adjacent normal tissues, we found that eightl ncRNAs were aberrantly expressed in HCC compared with corresponding NT, which is consistent with microarray data. Additionally, change trends of seven lncRNAs were basically identical to their nearby coding genes. In this study, to explore the potential involvement of lncRNAs in hepatocellular carcinoma (HCC) oncogenesis, we conducted lncRNA and mRNA profiling in 3 pairs of human HCC and adjacent normal tissue (NT) by microarray.

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