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Article: TCGA whole-transcriptome sequencing data reveals significantly dysregulated genes and signaling pathways in hepatocellular carcinoma

TitleTCGA whole-transcriptome sequencing data reveals significantly dysregulated genes and signaling pathways in hepatocellular carcinoma
Authors
Ho, DWHKai, AKLNg, IOL
KeywordsTCGA
HCC
liver cancer
whole-transcriptome sequencing
Issue Date2015
PublisherHigher Education Press. The Journal's web site is located at http://www.springer.com/medicine/journal/11684
Citation
Frontiers of Medicine, 2015, v. 9, n. 3, p. 322-330 How to Cite?
DOI: http://dx.doi.org/10.1007/s11684-015-0408-9
AbstractThis study systematically evaluates the TCGA whole-transcriptome sequencing data of hepatocellular carcinoma (HCC) by comparing the global gene expression profiles between tumors and their corresponding nontumorous liver tissue. Based on the differential gene expression analysis, we identified a number of novel dysregulated genes, in addition to those previously reported. Top-listing upregulated (CENPF and FOXM1) and downregulated (CLEC4G, CRHBP, and CLEC1B) genes were successfully validated using qPCR on our cohort of 65 pairs of human HCCs. Further examination for the mechanistic overview by subjecting significantly upregulated and downregulated genes to gene set enrichment analysis showed that different cellular pathways were involved. This study provides useful information on the transcriptomic landscape and molecular mechanism of hepatocarcinogenesis for development of new biomarkers and further in-depth characterization.
Persistent Identifierhttp://hdl.handle.net/10722/212083
ISSN
2095-0217
2021 Impact Factor: 9.927
2020 SCImago Journal Rankings: 1.240
ISI Accession Number ID
WOS:000368445200006

 

DC FieldValueLanguage
dc.contributor.authorHo, DWH-
dc.contributor.authorKai, AKL-
dc.contributor.authorNg, IOL-
dc.date.accessioned2015-07-21T02:22:26Z-
dc.date.available2015-07-21T02:22:26Z-
dc.date.issued2015-
dc.identifier.citationFrontiers of Medicine, 2015, v. 9, n. 3, p. 322-330-
dc.identifier.issn2095-0217-
dc.identifier.urihttp://hdl.handle.net/10722/212083-
dc.description.abstractThis study systematically evaluates the TCGA whole-transcriptome sequencing data of hepatocellular carcinoma (HCC) by comparing the global gene expression profiles between tumors and their corresponding nontumorous liver tissue. Based on the differential gene expression analysis, we identified a number of novel dysregulated genes, in addition to those previously reported. Top-listing upregulated (CENPF and FOXM1) and downregulated (CLEC4G, CRHBP, and CLEC1B) genes were successfully validated using qPCR on our cohort of 65 pairs of human HCCs. Further examination for the mechanistic overview by subjecting significantly upregulated and downregulated genes to gene set enrichment analysis showed that different cellular pathways were involved. This study provides useful information on the transcriptomic landscape and molecular mechanism of hepatocarcinogenesis for development of new biomarkers and further in-depth characterization.-
dc.languageeng-
dc.publisherHigher Education Press. The Journal's web site is located at http://www.springer.com/medicine/journal/11684-
dc.relation.ispartofFrontiers of Medicine-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectTCGA-
dc.subjectHCC-
dc.subjectliver cancer-
dc.subjectwhole-transcriptome sequencing-
dc.titleTCGA whole-transcriptome sequencing data reveals significantly dysregulated genes and signaling pathways in hepatocellular carcinoma-
dc.typeArticle-
dc.identifier.emailHo, DWH: dwhho@hku.hk-
dc.identifier.emailKai, AKL: klakai@hku.hk-
dc.identifier.emailNg, IOL: iolng@hku.hk-
dc.identifier.authorityNg, IOL=rp00335-
dc.identifier.doi10.1007/s11684-015-0408-9-
dc.identifier.pmid26276037-
dc.identifier.scopuseid_2-s2.0-84973434305-
dc.identifier.hkuros244516-
dc.identifier.volume9-
dc.identifier.issue3-
dc.identifier.spage322-
dc.identifier.epage330-
dc.identifier.isiWOS:000368445200006-
dc.publisher.placeBerlin-
dc.identifier.issnl2095-0217-

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