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Article: Unique and overlapping GLI1 and GLI2 transcriptional targets in neoplastic chondrocytes

TitleUnique and overlapping GLI1 and GLI2 transcriptional targets in neoplastic chondrocytes
Authors
Issue Date2019
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
PLoS One, 2019, v. 14 n. 1, article no. e0211333, p. 1-15 How to Cite?
AbstractExcessive Hedgehog (Hh) signaling in chondrocytes is sufficient to cause formation of enchondroma-like lesions which can progress to chondrosarcoma. To elucidate potential underlying mechanisms, we identified GLI1 and GLI2 target genes in human chondrosarcoma. Using chromatin immunoprecipitation (ChIP) sequencing and microarray data, in silico analyses were conducted to identify and characterize unique and overlapping GLI1 and GLI2 binding regions in neoplastic chondrocytes. After overlaying microarray data from human chondrosarcoma, 204 upregulated and 106 downregulated genes were identified as Hh-responsive Gli binding targets. After overlaying published Gli ChIP-on-chip data from mouse, 48 genes were identified as potential direct downstream targets of Hedgehog signaling with shared GLI binding regions in evolutionarily conserved DNA elements. Among these was BMP2, pointing to potential cross-talk between TGF beta signaling and Hh signaling. Our identification of potential target genes that are unique and common to GLI1 and GLI2 in neoplastic chondrocytes contributes to elucidating potential pathways through which Hh signaling impacts cartilage tumor biology.
Persistent Identifierhttp://hdl.handle.net/10722/268275
ISSN
2017 Impact Factor: 2.766
2015 SCImago Journal Rankings: 1.395
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorAli, SA-
dc.contributor.authorNiu, B-
dc.contributor.authorCheah, KSE-
dc.contributor.authorAlman, B-
dc.date.accessioned2019-03-18T04:22:14Z-
dc.date.available2019-03-18T04:22:14Z-
dc.date.issued2019-
dc.identifier.citationPLoS One, 2019, v. 14 n. 1, article no. e0211333, p. 1-15-
dc.identifier.issn1932-6203-
dc.identifier.urihttp://hdl.handle.net/10722/268275-
dc.description.abstractExcessive Hedgehog (Hh) signaling in chondrocytes is sufficient to cause formation of enchondroma-like lesions which can progress to chondrosarcoma. To elucidate potential underlying mechanisms, we identified GLI1 and GLI2 target genes in human chondrosarcoma. Using chromatin immunoprecipitation (ChIP) sequencing and microarray data, in silico analyses were conducted to identify and characterize unique and overlapping GLI1 and GLI2 binding regions in neoplastic chondrocytes. After overlaying microarray data from human chondrosarcoma, 204 upregulated and 106 downregulated genes were identified as Hh-responsive Gli binding targets. After overlaying published Gli ChIP-on-chip data from mouse, 48 genes were identified as potential direct downstream targets of Hedgehog signaling with shared GLI binding regions in evolutionarily conserved DNA elements. Among these was BMP2, pointing to potential cross-talk between TGF beta signaling and Hh signaling. Our identification of potential target genes that are unique and common to GLI1 and GLI2 in neoplastic chondrocytes contributes to elucidating potential pathways through which Hh signaling impacts cartilage tumor biology.-
dc.languageeng-
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action-
dc.relation.ispartofPLoS One-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleUnique and overlapping GLI1 and GLI2 transcriptional targets in neoplastic chondrocytes-
dc.typeArticle-
dc.identifier.emailNiu, B: csniuben@hku.hk-
dc.identifier.emailCheah, KSE: hrmbdkc@hku.hk-
dc.identifier.authorityCheah, KSE=rp00342-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0211333-
dc.identifier.pmid30695055-
dc.identifier.pmcidPMC6350985-
dc.identifier.scopuseid_2-s2.0-85060828378-
dc.identifier.hkuros297031-
dc.identifier.volume14-
dc.identifier.issue1-
dc.identifier.spagearticle no. e0211333, p. 1-
dc.identifier.epagearticle no. e0211333, p. 15-
dc.identifier.isiWOS:000457046400025-
dc.publisher.placeUnited States-

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