PubMed:23558898 JSON TXT

Annnotations TAB JSON ListView MergeView

sentences

DisGeNET

Allie

{"project":"Allie","denotations":[{"id":"SS1_23558898_2_0","span":{"begin":185,"end":193},"obj":"expanded"},{"id":"SS2_23558898_2_0","span":{"begin":195,"end":200},"obj":"abbr"},{"id":"SS1_23558898_2_1","span":{"begin":241,"end":253},"obj":"expanded"},{"id":"SS2_23558898_2_1","span":{"begin":255,"end":262},"obj":"abbr"},{"id":"SS1_23558898_2_2","span":{"begin":299,"end":338},"obj":"expanded"},{"id":"SS2_23558898_2_2","span":{"begin":340,"end":345},"obj":"abbr"},{"id":"SS1_23558898_3_0","span":{"begin":582,"end":619},"obj":"expanded"},{"id":"SS2_23558898_3_0","span":{"begin":621,"end":626},"obj":"abbr"},{"id":"SS1_23558898_12_0","span":{"begin":1481,"end":1502},"obj":"expanded"},{"id":"SS2_23558898_12_0","span":{"begin":1504,"end":1509},"obj":"abbr"}],"relations":[{"id":"AE1_23558898_2_0","pred":"abbreviatedTo","subj":"SS1_23558898_2_0","obj":"SS2_23558898_2_0"},{"id":"AE1_23558898_2_1","pred":"abbreviatedTo","subj":"SS1_23558898_2_1","obj":"SS2_23558898_2_1"},{"id":"AE1_23558898_2_2","pred":"abbreviatedTo","subj":"SS1_23558898_2_2","obj":"SS2_23558898_2_2"},{"id":"AE1_23558898_3_0","pred":"abbreviatedTo","subj":"SS1_23558898_3_0","obj":"SS2_23558898_3_0"},{"id":"AE1_23558898_12_0","pred":"abbreviatedTo","subj":"SS1_23558898_12_0","obj":"SS2_23558898_12_0"}],"text":"Tumour-suppressive microRNA-874 contributes to cell proliferation through targeting of histone deacetylase 1 in head and neck squamous cell carcinoma.\nBACKGROUND: Our recent studies of microRNA (miRNA) expression signature demonstrated that microRNA-874 (miR-874) was significantly downregulated in maxillary sinus squamous cell carcinoma (MSSCC), and a putative tumour-suppressive miRNA in human cancers. Our aim of this study was to investigate the functional significance of miR-874 in cancer cells and to identify novel miR-874-mediated cancer pathways and responsible genes in head and neck squamous cell carcinoma (HNSCC).\nMETHODS: Gain-of-function studies using mature miR-874 were performed to investigate cell proliferation and cell cycle distribution in HNSCC cell lines (SAS and FaDu). To identify miR-874-mediated molecular pathways and targets, we utilised gene expression analysis and in silico database analysis. Loss-of-function assays were performed to investigate the functional significance of miR-874 target genes.\nRESULTS: Expression levels of miR-874 were significantly downregulated in HNSCC tissues (including oral, pharyngeal and laryngeal SCCs) compared with normal counterpart epithelia. Restoration of miR-874 in SAS and FaDu cell lines revealed significant inhibition of cell proliferation and induction of G2/M arrest and cell apoptosis. Our expression data and in silico analysis demonstrated that miR-874 modulated the cell cycle pathway. Moreover, histone deacetylase 1 (HDAC1) was a candidate target of miR-874 regulation. Luciferase reporter assays showed that miR-874 directly regulated HDAC1. Silencing of the HDAC1 gene significantly inhibited cell proliferation and induced G2/M arrest and cell apoptosis in SAS cells.\nCONCLUSIONS: Downregulation of miR-874 was a frequent event in HNSCC. miR-874 acted as a tumour suppressor and directly targeted HDAC1. Recognition of tumour-suppressive miRNA-mediated cancer pathways provides new insights into the potential mechanisms of HNSCC oncogenesis and suggests novel therapeutic strategies for the disease."}

PubmedHPO

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":315,"end":338},"obj":"HP_0002860"},{"id":"T2","span":{"begin":363,"end":369},"obj":"HP_0002664"},{"id":"T3","span":{"begin":397,"end":404},"obj":"HP_0002664"},{"id":"T4","span":{"begin":489,"end":495},"obj":"HP_0002664"},{"id":"T5","span":{"begin":541,"end":547},"obj":"HP_0002664"},{"id":"T6","span":{"begin":596,"end":619},"obj":"HP_0002860"}],"text":"Tumour-suppressive microRNA-874 contributes to cell proliferation through targeting of histone deacetylase 1 in head and neck squamous cell carcinoma.\nBACKGROUND: Our recent studies of microRNA (miRNA) expression signature demonstrated that microRNA-874 (miR-874) was significantly downregulated in maxillary sinus squamous cell carcinoma (MSSCC), and a putative tumour-suppressive miRNA in human cancers. Our aim of this study was to investigate the functional significance of miR-874 in cancer cells and to identify novel miR-874-mediated cancer pathways and responsible genes in head and neck squamous cell carcinoma (HNSCC).\nMETHODS: Gain-of-function studies using mature miR-874 were performed to investigate cell proliferation and cell cycle distribution in HNSCC cell lines (SAS and FaDu). To identify miR-874-mediated molecular pathways and targets, we utilised gene expression analysis and in silico database analysis. Loss-of-function assays were performed to investigate the functional significance of miR-874 target genes.\nRESULTS: Expression levels of miR-874 were significantly downregulated in HNSCC tissues (including oral, pharyngeal and laryngeal SCCs) compared with normal counterpart epithelia. Restoration of miR-874 in SAS and FaDu cell lines revealed significant inhibition of cell proliferation and induction of G2/M arrest and cell apoptosis. Our expression data and in silico analysis demonstrated that miR-874 modulated the cell cycle pathway. Moreover, histone deacetylase 1 (HDAC1) was a candidate target of miR-874 regulation. Luciferase reporter assays showed that miR-874 directly regulated HDAC1. Silencing of the HDAC1 gene significantly inhibited cell proliferation and induced G2/M arrest and cell apoptosis in SAS cells.\nCONCLUSIONS: Downregulation of miR-874 was a frequent event in HNSCC. miR-874 acted as a tumour suppressor and directly targeted HDAC1. Recognition of tumour-suppressive miRNA-mediated cancer pathways provides new insights into the potential mechanisms of HNSCC oncogenesis and suggests novel therapeutic strategies for the disease."}

DisGeNET5_gene_disease

DisGeNet-2017-sample

{"project":"DisGeNet-2017-sample","denotations":[{"id":"T2678","span":{"begin":782,"end":785},"obj":"gene:54187"},{"id":"T2679","span":{"begin":764,"end":769},"obj":"disease:C1168401"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T2678","obj":"T2679"},{"id":"R2","pred":"associated_with","subj":"T2678","obj":"T2679"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Tumour-suppressive microRNA-874 contributes to cell proliferation through targeting of histone deacetylase 1 in head and neck squamous cell carcinoma.\nBACKGROUND: Our recent studies of microRNA (miRNA) expression signature demonstrated that microRNA-874 (miR-874) was significantly downregulated in maxillary sinus squamous cell carcinoma (MSSCC), and a putative tumour-suppressive miRNA in human cancers. Our aim of this study was to investigate the functional significance of miR-874 in cancer cells and to identify novel miR-874-mediated cancer pathways and responsible genes in head and neck squamous cell carcinoma (HNSCC).\nMETHODS: Gain-of-function studies using mature miR-874 were performed to investigate cell proliferation and cell cycle distribution in HNSCC cell lines (SAS and FaDu). To identify miR-874-mediated molecular pathways and targets, we utilised gene expression analysis and in silico database analysis. Loss-of-function assays were performed to investigate the functional significance of miR-874 target genes.\nRESULTS: Expression levels of miR-874 were significantly downregulated in HNSCC tissues (including oral, pharyngeal and laryngeal SCCs) compared with normal counterpart epithelia. Restoration of miR-874 in SAS and FaDu cell lines revealed significant inhibition of cell proliferation and induction of G2/M arrest and cell apoptosis. Our expression data and in silico analysis demonstrated that miR-874 modulated the cell cycle pathway. Moreover, histone deacetylase 1 (HDAC1) was a candidate target of miR-874 regulation. Luciferase reporter assays showed that miR-874 directly regulated HDAC1. Silencing of the HDAC1 gene significantly inhibited cell proliferation and induced G2/M arrest and cell apoptosis in SAS cells.\nCONCLUSIONS: Downregulation of miR-874 was a frequent event in HNSCC. miR-874 acted as a tumour suppressor and directly targeted HDAC1. Recognition of tumour-suppressive miRNA-mediated cancer pathways provides new insights into the potential mechanisms of HNSCC oncogenesis and suggests novel therapeutic strategies for the disease."}

UBERON-AE

{"project":"UBERON-AE","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":112,"end":116},"obj":"http://purl.obolibrary.org/obo/UBERON_0000033"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":582,"end":586},"obj":"http://purl.obolibrary.org/obo/UBERON_0000033"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":121,"end":125},"obj":"http://purl.obolibrary.org/obo/UBERON_0000974"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":591,"end":595},"obj":"http://purl.obolibrary.org/obo/UBERON_0000974"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":299,"end":314},"obj":"http://purl.obolibrary.org/obo/UBERON_0001764"},{"id":"PD-UBERON-AE-B_T6","span":{"begin":1115,"end":1122},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"}],"text":"Tumour-suppressive microRNA-874 contributes to cell proliferation through targeting of histone deacetylase 1 in head and neck squamous cell carcinoma.\nBACKGROUND: Our recent studies of microRNA (miRNA) expression signature demonstrated that microRNA-874 (miR-874) was significantly downregulated in maxillary sinus squamous cell carcinoma (MSSCC), and a putative tumour-suppressive miRNA in human cancers. Our aim of this study was to investigate the functional significance of miR-874 in cancer cells and to identify novel miR-874-mediated cancer pathways and responsible genes in head and neck squamous cell carcinoma (HNSCC).\nMETHODS: Gain-of-function studies using mature miR-874 were performed to investigate cell proliferation and cell cycle distribution in HNSCC cell lines (SAS and FaDu). To identify miR-874-mediated molecular pathways and targets, we utilised gene expression analysis and in silico database analysis. Loss-of-function assays were performed to investigate the functional significance of miR-874 target genes.\nRESULTS: Expression levels of miR-874 were significantly downregulated in HNSCC tissues (including oral, pharyngeal and laryngeal SCCs) compared with normal counterpart epithelia. Restoration of miR-874 in SAS and FaDu cell lines revealed significant inhibition of cell proliferation and induction of G2/M arrest and cell apoptosis. Our expression data and in silico analysis demonstrated that miR-874 modulated the cell cycle pathway. Moreover, histone deacetylase 1 (HDAC1) was a candidate target of miR-874 regulation. Luciferase reporter assays showed that miR-874 directly regulated HDAC1. Silencing of the HDAC1 gene significantly inhibited cell proliferation and induced G2/M arrest and cell apoptosis in SAS cells.\nCONCLUSIONS: Downregulation of miR-874 was a frequent event in HNSCC. miR-874 acted as a tumour suppressor and directly targeted HDAC1. Recognition of tumour-suppressive miRNA-mediated cancer pathways provides new insights into the potential mechanisms of HNSCC oncogenesis and suggests novel therapeutic strategies for the disease."}

performance-test

{"project":"performance-test","denotations":[{"id":"PD-UBERON-AE-B_T1","span":{"begin":1115,"end":1122},"obj":"http://purl.obolibrary.org/obo/UBERON_0000479"},{"id":"PD-UBERON-AE-B_T2","span":{"begin":112,"end":116},"obj":"http://purl.obolibrary.org/obo/UBERON_0000033"},{"id":"PD-UBERON-AE-B_T3","span":{"begin":582,"end":586},"obj":"http://purl.obolibrary.org/obo/UBERON_0000033"},{"id":"PD-UBERON-AE-B_T4","span":{"begin":121,"end":125},"obj":"http://purl.obolibrary.org/obo/UBERON_0000974"},{"id":"PD-UBERON-AE-B_T5","span":{"begin":591,"end":595},"obj":"http://purl.obolibrary.org/obo/UBERON_0000974"},{"id":"PD-UBERON-AE-B_T6","span":{"begin":299,"end":314},"obj":"http://purl.obolibrary.org/obo/UBERON_0001764"}],"text":"Tumour-suppressive microRNA-874 contributes to cell proliferation through targeting of histone deacetylase 1 in head and neck squamous cell carcinoma.\nBACKGROUND: Our recent studies of microRNA (miRNA) expression signature demonstrated that microRNA-874 (miR-874) was significantly downregulated in maxillary sinus squamous cell carcinoma (MSSCC), and a putative tumour-suppressive miRNA in human cancers. Our aim of this study was to investigate the functional significance of miR-874 in cancer cells and to identify novel miR-874-mediated cancer pathways and responsible genes in head and neck squamous cell carcinoma (HNSCC).\nMETHODS: Gain-of-function studies using mature miR-874 were performed to investigate cell proliferation and cell cycle distribution in HNSCC cell lines (SAS and FaDu). To identify miR-874-mediated molecular pathways and targets, we utilised gene expression analysis and in silico database analysis. Loss-of-function assays were performed to investigate the functional significance of miR-874 target genes.\nRESULTS: Expression levels of miR-874 were significantly downregulated in HNSCC tissues (including oral, pharyngeal and laryngeal SCCs) compared with normal counterpart epithelia. Restoration of miR-874 in SAS and FaDu cell lines revealed significant inhibition of cell proliferation and induction of G2/M arrest and cell apoptosis. Our expression data and in silico analysis demonstrated that miR-874 modulated the cell cycle pathway. Moreover, histone deacetylase 1 (HDAC1) was a candidate target of miR-874 regulation. Luciferase reporter assays showed that miR-874 directly regulated HDAC1. Silencing of the HDAC1 gene significantly inhibited cell proliferation and induced G2/M arrest and cell apoptosis in SAS cells.\nCONCLUSIONS: Downregulation of miR-874 was a frequent event in HNSCC. miR-874 acted as a tumour suppressor and directly targeted HDAC1. Recognition of tumour-suppressive miRNA-mediated cancer pathways provides new insights into the potential mechanisms of HNSCC oncogenesis and suggests novel therapeutic strategies for the disease."}