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Article: The molecular differences between human papillomavirus-positive and -negative oropharyngeal squamous cell carcinoma: A bioinformatics study

TitleThe molecular differences between human papillomavirus-positive and -negative oropharyngeal squamous cell carcinoma: A bioinformatics study
Authors
KeywordsHuman papillomavirus
Oropharyngeal squamous cell carcinoma
Genes
miRNAs
Pathways
Issue Date2019
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/amjoto
Citation
American Journal of Otolaryngology, 2019, v. 40 n. 4, p. 547-554 How to Cite?
AbstractObjective: To investigate the genetic and epigenetic differences between human papillomavirus (HPV)-positive oropharyngeal squamous cell carcinoma (OPSCC) and HPV-negative OPSCC. Methods: Microarray data of HPV-positive and -negative OPSCC were retrieved from NCBI GEO datasets. Differentially expressed genes (DEGs) and differentially expressed miRNAs (DE-miRNAs) were identified by performing differential expression analysis. A functional enrichment analysis was performed to explore the biological processes and signaling pathways that DEGs and DE-miRNAs were involved in, respectively. A protein-protein interaction (PPI) network of DEGs was constructed to identify hub genes. miRNA-target network and miRNA-miRNA functional synergistic network were each constructed in order to identify risk-marker miRNAs. An miRNA-target-pathway network was constructed in order to explore the function of identified risk-marker miRNAs. Results: Microarray data from 3 datasets (GSE39366, GSE40774, and GSE55550) was included and analyzed. The PPI network identified 3 hub genes (VCAM1, UBD, and RPA2). MiR-107 and miR-142-3p were found to play the most significant role in both the DE-miRNA-target network as well as in the miRNA-miRNA functional synergistic network. MiR-107 was involved in HPV-induced tumorigenesis by targeting many genes (CAV1, CDK6, MYB, and SERPINB5) and regulating the p53 signaling pathway, the PI3K-Akt signaling pathway, and the autophagy pathway. In addition, miR-142-3p was implicated in HPV-induced tumorigenesis by targeting the PPFIA1 gene and regulating transcriptional dysregulation and other cancerous pathways. Conclusion: Three genes (VCAM1, UBD, and RPA2), two miRNAs (miR-107 and miR-142-3p), and four pathways (p53, PI3K-Akt, autophagy, and transcription dysregulation in cancer) were identified to play critical roles in distinguishing HPV-positive OPSCC from HPV-negative OPSCC.
Persistent Identifierhttp://hdl.handle.net/10722/279131
ISSN
2017 Impact Factor: 1.046
2015 SCImago Journal Rankings: 0.590

 

DC FieldValueLanguage
dc.contributor.authorWang, J-
dc.contributor.authorXi, X-
dc.contributor.authorShang, W-
dc.contributor.authorAcharya, A-
dc.contributor.authorLi, S-
dc.contributor.authorSavkovic, V-
dc.contributor.authorLi, H-
dc.contributor.authorHaak, R-
dc.contributor.authorSchmidt, J-
dc.contributor.authorLiu, X-
dc.contributor.authorDeng, Y-
dc.contributor.authorPan, H-
dc.contributor.authorObradovic, D-
dc.contributor.authorSchmalz, G-
dc.contributor.authorZiebolz, D-
dc.contributor.authorHu, X-
dc.date.accessioned2019-10-21T02:20:09Z-
dc.date.available2019-10-21T02:20:09Z-
dc.date.issued2019-
dc.identifier.citationAmerican Journal of Otolaryngology, 2019, v. 40 n. 4, p. 547-554-
dc.identifier.issn0196-0709-
dc.identifier.urihttp://hdl.handle.net/10722/279131-
dc.description.abstractObjective: To investigate the genetic and epigenetic differences between human papillomavirus (HPV)-positive oropharyngeal squamous cell carcinoma (OPSCC) and HPV-negative OPSCC. Methods: Microarray data of HPV-positive and -negative OPSCC were retrieved from NCBI GEO datasets. Differentially expressed genes (DEGs) and differentially expressed miRNAs (DE-miRNAs) were identified by performing differential expression analysis. A functional enrichment analysis was performed to explore the biological processes and signaling pathways that DEGs and DE-miRNAs were involved in, respectively. A protein-protein interaction (PPI) network of DEGs was constructed to identify hub genes. miRNA-target network and miRNA-miRNA functional synergistic network were each constructed in order to identify risk-marker miRNAs. An miRNA-target-pathway network was constructed in order to explore the function of identified risk-marker miRNAs. Results: Microarray data from 3 datasets (GSE39366, GSE40774, and GSE55550) was included and analyzed. The PPI network identified 3 hub genes (VCAM1, UBD, and RPA2). MiR-107 and miR-142-3p were found to play the most significant role in both the DE-miRNA-target network as well as in the miRNA-miRNA functional synergistic network. MiR-107 was involved in HPV-induced tumorigenesis by targeting many genes (CAV1, CDK6, MYB, and SERPINB5) and regulating the p53 signaling pathway, the PI3K-Akt signaling pathway, and the autophagy pathway. In addition, miR-142-3p was implicated in HPV-induced tumorigenesis by targeting the PPFIA1 gene and regulating transcriptional dysregulation and other cancerous pathways. Conclusion: Three genes (VCAM1, UBD, and RPA2), two miRNAs (miR-107 and miR-142-3p), and four pathways (p53, PI3K-Akt, autophagy, and transcription dysregulation in cancer) were identified to play critical roles in distinguishing HPV-positive OPSCC from HPV-negative OPSCC.-
dc.languageeng-
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/amjoto-
dc.relation.ispartofAmerican Journal of Otolaryngology-
dc.subjectHuman papillomavirus-
dc.subjectOropharyngeal squamous cell carcinoma-
dc.subjectGenes-
dc.subjectmiRNAs-
dc.subjectPathways-
dc.titleThe molecular differences between human papillomavirus-positive and -negative oropharyngeal squamous cell carcinoma: A bioinformatics study-
dc.typeArticle-
dc.identifier.emailAcharya, A: aneesha@hku.hk-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.amjoto.2019.04.015-
dc.identifier.pmid31036418-
dc.identifier.scopuseid_2-s2.0-85064601254-
dc.identifier.hkuros307571-
dc.identifier.volume40-
dc.identifier.issue4-
dc.identifier.spage547-
dc.identifier.epage554-
dc.publisher.placeUnited States-

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