Nuclear Pirin promotes HCC by acting as a key inflammation-facilitating factor
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ABSTRACT:
PROVIDER: PRJNA1002341 | ENA |
REPOSITORIES: ENA
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Project description:HCC has a poor response to therapy and a bad prognosis with chronic inflammation be the most common etiologies for HCC progression. Here we report a redox-dependent regulation mechanism of PIR protein nuclear shuttling, leading to liver inflammation and HCC progression.
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Project description:Globally, hepatocellular carcinoma (HCC) accounts for 70-85% of primary liver cancers and is the second leading cause of male cancer death. Among patients with HCC there is widespread heterogeneity, yet just a single standard therapeutic, Sorafenib, which is only effective in patients with overactive MAP kinase signaling. Identifying homogeneous subgroups of HCC patients will improve our ability to develop more effective targeted treatment modalities derived from specific signaling pathways that lead to poor survival. Recently, many 'omics based studies have further described the current problem of cancer heterogeneity. Genomics is the application of high-throughput methods to analyze the expression of genes at a global level, while epigenomics focuses on epigenetic modifications, such as DNA methylation changes, across the genome. Though genome-wide analysis by various 'omics methods is popular, the integration of the data is uncommon. We hypothesize that the integration of patient expression data will reveal distinct epigenetic and genomic modifications in subsets of HCC patients that lead to poor outcome. In this study, we employed Illumina or Affymetrix array platforms to analyze paired tumor and non-tumor tissue specimens from 82 HCC patients in an integrative approach incorporating DNA methylation, somatic DNA copy number alteration (SCNA) and expression of mRNA and microRNA genes. First we performed a class comparison analysis between tumor and non-tumor patients to identify 2,173 differentially methylated genes (Illumina 27k BeadChip). Of those genes, only 621 overlapped with tumor-specific genes differentially expressed in the same patients (Affymetrix array). We further narrowed that tumor-specific gene list by removing only a subset of genes that correlated with methylation data. An epigenetic-driven gene signature of 46 genes was established using a correlation coefficient of -0.185 corresponding to the 95th percentile of the 1000-fold random distribution. In a similar manner, an SCNA-related gene signature made up of 2,722 tumor-specific genes was established using a correlation coefficient of 0.3 corresponding to the 99th percentile of the 1000-fold random distribution. The gene signatures do not significantly overlap and each has the ability to cluster HCC patients with poor outcome apart from patients with better prognosis. Moving forward, we plan to focus on key signaling pathways derived from integrated gene and miRNA expression data that are responsible for poor prognosis in patients. Upon identification, driver pathways will be validated in vitro and in vivo to elucidate the mechanisms of HCC progression and poor outcome.
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Project description:The variability in the prognosis of hepatocellular carcinoma (HCC) patients suggests that HCC may comprise several distinctive biological phenotypes. These phenotypes may result from different neoplastic pathways during the tumorigenesis and/or from a different cell of origin. Here we address if the transcriptional characteristics of the HCC would provide insight into the cellular origin of the tumors. We integrated gene expression data from rat fetal hepatoblasts and adult hepatocytes, HCC from mouse models, and human HCC. The HCC patients who shared gene expression patterns with fetal hepatoblasts showed extremely poor prognosis when compared with those lacking the hepatoblast signature. The gene expression program that distinguishes this novel subtype from the rest of HCC includes well known markers of hepatic oval cells, suggesting that HCC in this subtype may arise from hepatic progenitor cells. Two independent gene network analyses of the gene expression signature characteristic for the tumors sharing the hepatoblast expression patterns revealed that activation of AP-1 transcription factors might play key roles in tumor development in the newly identified HCC subtype. In addition, by applying hepatoblast-specific and genome-wide global signatures, HCC patients were further stratified into three distinct subgroups with a significant association with overall survival and recurrence. Keywords: individual genetic characteristic design
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Project description:RNA-sequencing of Human hepatocellular carcinoma (HCC) cells We analyzed two circRNA profiles expressed in human HCC tissues and identified circRHOT1 as a conserved and dramatically upregulated circRNA in HCC tissues. HCC patients displaying high circRHOT1 level possessed poor prognosis. We demonstrated circRHOT1 significantly promoted HCC growth and metastasis. In order to investigate the mechansim of circRHOT1, we constructed circRHOT1-deficient HCC cell lines. Through RNA-sequencing, we sough to identify the key gene regulated by circRHOT1 in HCC.
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Project description:Although many protein-coding genes have been identified to be aberrantly expressed in hepatocellular carcinoma (HCC), the mechanisms that account for development and progression of HCC remain unclear. In recent years, long noncoding RNAs (lncRNAs) have been shown to have critical regulatory roles in mammalian cell biology. Many lncRNAs can result in aberrant expression of gene products that may contribute to cancer biology. In this study, we first identified non-overlapping signatures of a small number of lncRNAs that are aberrantly expressed in human HCC compared with paired peritumoral tissues. Then we used real-time PCR to validate five lncRNAs whose expression was altered in HCC compared with paired peritumoral tissues. Using loss-of-function and gain-of-function approaches, we found that an lncRNA (termed lncRNA-HEIH) plays a key role in cell cycle regulation. We further demonstrated that lncRNA-HEIH bound to enhancer of zeste homolog 2 (EZH2) and that this interaction was required for the repression of EZH2 target genes. Together, these results reveal insights into the molecular regulation mechanisms of HCC cell cycle regulation and lead us to propose that lncRNAs may serve as key regulatory hubs in cancer biology. A ten chip study using total RNA recovered from five separate HCC tissues and five corresponding paired non-tumor samples.
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