Integrative epigenomic profiling of hepatocellular carcinoma uncovers aberrant cis-regulatory changes and potential prognostic indicators [ChIP-seq]
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ABSTRACT:
PROVIDER: PRJNA1154966 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR30502722.fastq.gz | Fastqsanger.gz | |||
| SRR30502723.fastq.gz | Fastqsanger.gz | |||
| SRR30502724.fastq.gz | Fastqsanger.gz | |||
| SRR30502725.fastq.gz | Fastqsanger.gz | |||
| SRR30502725_1.fastq.gz | Fastqsanger.gz |
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Project description:Integrative epigenomic profiling of hepatocellular carcinoma uncovers aberrant cis-regulatory changes and potential prognostic indicators [RNA-seq]
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Project description:Hepatocellular carcinoma (HCC) exhibits widespread epigenetic aberrations; however, the underlying transcriptional regulatory landscape remains underexplored. Here, we performed integrated analyses with genome-wide profiles of the transcriptomes, histone modifications and DNA methylation from patient-derived HCC tumors and controls. We identified both global and focal epigenetic alterations including large-scale DNA methylation loss, and dysregulation of cis-regulatory elements (CREs) associated with genes involved in cell cycle control, immune responses, and extracellular matrix organization. Notably, we discovered that transcriptional upregulation of Glypican-3 (GPC3), a diagnostic biomarker and immunotherapeutic target for HCC, was linked to the reactivation of a fetal liver super-enhancer (SE). This SE, in concert with DNA hypomethylation of two CpG islands, modulated GPC3 expression. Global DNA hypomethylation also contributed to transcriptional dysregulation of retrotransposon-derived CREs. Specifically, we observed that patients with high expression of a HERVE-int-driven long non-coding RNA transcript showed poorer disease outcomes and specific molecular signatures associated with better response to immunotherapy. Our results highlight this and other retrotransposons as potential prognostic indicators and a predictive signature for immunotherapy response. Taken together, our findings provide insights into the role of epigenetic dysregulation of CREs and retrotransposons in hepatocarcinogenesis, which could benefit the clinical management of HCC.
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Project description:Hepatocellular carcinoma (HCC) exhibits widespread epigenetic aberrations; however, the underlying transcriptional regulatory landscape remains underexplored. Here, we performed integrated analyses with genome-wide profiles of the transcriptomes, histone modifications and DNA methylation from patient-derived HCC tumors and controls. We identified both global and focal epigenetic alterations including large-scale DNA methylation loss, and dysregulation of cis-regulatory elements (CREs) associated with genes involved in cell cycle control, immune responses, and extracellular matrix organization. Notably, we discovered that transcriptional upregulation of Glypican-3 (GPC3), a diagnostic biomarker and immunotherapeutic target for HCC, was linked to the reactivation of a fetal liver super-enhancer (SE). This SE, in concert with DNA hypomethylation of two CpG islands, modulated GPC3 expression. Global DNA hypomethylation also contributed to transcriptional dysregulation of retrotransposon-derived CREs. Specifically, we observed that patients with high expression of a HERVE-int-driven long non-coding RNA transcript showed poorer disease outcomes and specific molecular signatures associated with better response to immunotherapy. Our results highlight this and other retrotransposons as potential prognostic indicators and a predictive signature for immunotherapy response. Taken together, our findings provide insights into the role of epigenetic dysregulation of CREs and retrotransposons in hepatocarcinogenesis, which could benefit the clinical management of HCC.
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Project description:Background: Long noncoding RNAs (lncRNAs) are pervasively transcribed and play a key role in tumorigenesis. The aim of the present study was to determine the lncRNA expression profile in astrocytoma patients and to assess the potential clinical value of the findings. Methods: The global lncRNA expression profile in astrocytoma was measured by lncRNA microarray. Next, the differentially expressed lncRNAs were validated using a Taqman probe-based quantitative real time-PCR (qRT-PCR) assay in 130 astrocytoma and 60 normal adjacent tissue (NAT) samples, which were randomly divided into a training set and a validation set. Finally, the correlation of the lncRNA levels with survival of the astrocytoma patients was estimated by performing a Kaplan-Meier survival analysis and a univariate/multivariate Cox proportional hazard regression analysis. Results: After a two-phase selection and validation process, 7 lncRNAs were found to have a significantly different expression profile in astrocytoma samples compared to the NAT samples. Unsupervised clustering analysis further revealed the potential of the 7-lncRNA profile to differentiate between tumors and NAT samples. Using Kaplan-Meier survival analysis, we found that the low expression of XLOC_005285 and XLOC_010967 and the high expression of HIT000260843.11 were significantly associated with poor patient survival. Moreover, Cox proportional hazard regression analysis revealed that this prognostic impact was independent of other clinicopathological factors. The lncRNA expression profiles of 3 astrocytoma tissues and 3 normal adjacent tissues were studied by microarray.
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