PubMed:28346429 JSONTXT

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of endothelial cell-specific liver kinase B1 increases angiogenesis and tumor growth via vascular endothelial growth factor.\nLiver kinase B1 (LKB1) is a serine/threonine protein kinase ubiquitously expressed in mammalian cells. It was first identified in Peutz-Jeghers syndrome as a tumor suppressor gene. Whether endothelial LKB1 regulates angiogenesis and tumor growth is unknown. In this study, we generated endothelial cell-specific LKB1-knockout (LKB1(endo-/-)) mice by crossbreeding vascular endothelial-cadherin-Cre mice with LKB1(flox/flox) mice. Vascular endothelial growth factor (VEGF) level was highly co-stained in endothelial cells but not in macrophages in LKB1(endo-/-) mice. Consistently, LKB1(endo-/-) mouse tissues including the lung, skin, kidney and liver showed increased vascular permeability. Tumors implanted in LKB1(endo-/-) mice but not macrophage-specific LKB1-knockout mice grew faster and showed enhanced vascular permeability and increased angiogenesis as compared with those implanted in wild-type mice. Injection of VEGF-neutralizing antibody but not the isotype-matched control antibody decreased endothelial-cell angiogenesis and tumor growth in vivo. Furthermore, LKB1 deletion enhanced mouse retinal and cell angiogenesis, and knockdown of VEGF by small-interfering RNA decreased endothelial cell proliferation and migration. Re-expression of LKB1 or knockdown of VEGF receptor 2 decreased the overproliferation and -migration observed in LKB1(endo-/-) cells. Mechanistically, LKB1 could bind to the VEGF transcription factor, specificity protein 1 (Sp1), which then inhibited the binding of Sp1 to the VEGF promoter to reduce VEGF expression. Endothelial LKB1 may regulate endothelial angiogenesis and tumor growth by modulating Sp1-mediated VEGF expression."}

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{"project":"LitCoin-Disease-MeSH","denotations":[{"id":"T1","span":{"begin":81,"end":86},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":264,"end":286},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":292,"end":297},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":367,"end":372},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":826,"end":832},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":1174,"end":1179},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":1749,"end":1754},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A6","pred":"originalLabel","subj":"T6","obj":"D009369"},{"id":"A3","pred":"originalLabel","subj":"T3","obj":"D009369"},{"id":"A1","pred":"originalLabel","subj":"T1","obj":"D009369"},{"id":"A2","pred":"originalLabel","subj":"T2","obj":"D010580"},{"id":"A7","pred":"originalLabel","subj":"T7","obj":"D009369"},{"id":"A5","pred":"originalLabel","subj":"T5","obj":"D009369"},{"id":"A4","pred":"originalLabel","subj":"T4","obj":"D009369"}],"text":"Deletion of endothelial cell-specific liver kinase B1 increases angiogenesis and tumor growth via vascular endothelial growth factor.\nLiver kinase B1 (LKB1) is a serine/threonine protein kinase ubiquitously expressed in mammalian cells. It was first identified in Peutz-Jeghers syndrome as a tumor suppressor gene. Whether endothelial LKB1 regulates angiogenesis and tumor growth is unknown. In this study, we generated endothelial cell-specific LKB1-knockout (LKB1(endo-/-)) mice by crossbreeding vascular endothelial-cadherin-Cre mice with LKB1(flox/flox) mice. Vascular endothelial growth factor (VEGF) level was highly co-stained in endothelial cells but not in macrophages in LKB1(endo-/-) mice. Consistently, LKB1(endo-/-) mouse tissues including the lung, skin, kidney and liver showed increased vascular permeability. Tumors implanted in LKB1(endo-/-) mice but not macrophage-specific LKB1-knockout mice grew faster and showed enhanced vascular permeability and increased angiogenesis as compared with those implanted in wild-type mice. Injection of VEGF-neutralizing antibody but not the isotype-matched control antibody decreased endothelial-cell angiogenesis and tumor growth in vivo. Furthermore, LKB1 deletion enhanced mouse retinal and cell angiogenesis, and knockdown of VEGF by small-interfering RNA decreased endothelial cell proliferation and migration. Re-expression of LKB1 or knockdown of VEGF receptor 2 decreased the overproliferation and -migration observed in LKB1(endo-/-) cells. Mechanistically, LKB1 could bind to the VEGF transcription factor, specificity protein 1 (Sp1), which then inhibited the binding of Sp1 to the VEGF promoter to reduce VEGF expression. Endothelial LKB1 may regulate endothelial angiogenesis and tumor growth by modulating Sp1-mediated VEGF expression."}

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{"project":"LitCoin_Mondo_095","denotations":[{"id":"T1","span":{"begin":81,"end":86},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":264,"end":286},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":292,"end":297},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":367,"end":372},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":757,"end":761},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":763,"end":767},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":1174,"end":1179},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":1749,"end":1754},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A7","pred":"mondo_id","subj":"T7","obj":"0005070"},{"id":"A3","pred":"mondo_id","subj":"T3","obj":"0005070"},{"id":"A5","pred":"mondo_id","subj":"T5","obj":"0021117"},{"id":"A6","pred":"mondo_id","subj":"T6","obj":"0002531"},{"id":"A1","pred":"mondo_id","subj":"T1","obj":"0005070"},{"id":"A8","pred":"mondo_id","subj":"T8","obj":"0005070"},{"id":"A2","pred":"mondo_id","subj":"T2","obj":"0008280"},{"id":"A4","pred":"mondo_id","subj":"T4","obj":"0005070"}],"text":"Deletion of endothelial cell-specific liver kinase B1 increases angiogenesis and tumor growth via vascular endothelial growth factor.\nLiver kinase B1 (LKB1) is a serine/threonine protein kinase ubiquitously expressed in mammalian cells. It was first identified in Peutz-Jeghers syndrome as a tumor suppressor gene. Whether endothelial LKB1 regulates angiogenesis and tumor growth is unknown. In this study, we generated endothelial cell-specific LKB1-knockout (LKB1(endo-/-)) mice by crossbreeding vascular endothelial-cadherin-Cre mice with LKB1(flox/flox) mice. Vascular endothelial growth factor (VEGF) level was highly co-stained in endothelial cells but not in macrophages in LKB1(endo-/-) mice. Consistently, LKB1(endo-/-) mouse tissues including the lung, skin, kidney and liver showed increased vascular permeability. Tumors implanted in LKB1(endo-/-) mice but not macrophage-specific LKB1-knockout mice grew faster and showed enhanced vascular permeability and increased angiogenesis as compared with those implanted in wild-type mice. Injection of VEGF-neutralizing antibody but not the isotype-matched control antibody decreased endothelial-cell angiogenesis and tumor growth in vivo. Furthermore, LKB1 deletion enhanced mouse retinal and cell angiogenesis, and knockdown of VEGF by small-interfering RNA decreased endothelial cell proliferation and migration. Re-expression of LKB1 or knockdown of VEGF receptor 2 decreased the overproliferation and -migration observed in LKB1(endo-/-) cells. Mechanistically, LKB1 could bind to the VEGF transcription factor, specificity protein 1 (Sp1), which then inhibited the binding of Sp1 to the VEGF promoter to reduce VEGF expression. Endothelial LKB1 may regulate endothelial angiogenesis and tumor growth by modulating Sp1-mediated VEGF expression."}

{"project":"LitCoin-MeSH-Disease-2","denotations":[{"id":"T1","span":{"begin":81,"end":86},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":264,"end":286},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":292,"end":297},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":367,"end":372},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":826,"end":832},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":1174,"end":1179},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T8","span":{"begin":1749,"end":1754},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A4","pred":"ID:","subj":"T4","obj":"D009369"},{"id":"A8","pred":"ID:","subj":"T8","obj":"D009369"},{"id":"A1","pred":"ID:","subj":"T1","obj":"D009369"},{"id":"A7","pred":"ID:","subj":"T7","obj":"D009369"},{"id":"A3","pred":"ID:","subj":"T3","obj":"D009369"},{"id":"A5","pred":"ID:","subj":"T5","obj":"DISEASE"},{"id":"A6","pred":"ID:","subj":"T5","obj":"D009369"},{"id":"A2","pred":"ID:","subj":"T2","obj":"D010580"}],"text":"Deletion of endothelial cell-specific liver kinase B1 increases angiogenesis and tumor growth via vascular endothelial growth factor.\nLiver kinase B1 (LKB1) is a serine/threonine protein kinase ubiquitously expressed in mammalian cells. It was first identified in Peutz-Jeghers syndrome as a tumor suppressor gene. Whether endothelial LKB1 regulates angiogenesis and tumor growth is unknown. In this study, we generated endothelial cell-specific LKB1-knockout (LKB1(endo-/-)) mice by crossbreeding vascular endothelial-cadherin-Cre mice with LKB1(flox/flox) mice. Vascular endothelial growth factor (VEGF) level was highly co-stained in endothelial cells but not in macrophages in LKB1(endo-/-) mice. Consistently, LKB1(endo-/-) mouse tissues including the lung, skin, kidney and liver showed increased vascular permeability. Tumors implanted in LKB1(endo-/-) mice but not macrophage-specific LKB1-knockout mice grew faster and showed enhanced vascular permeability and increased angiogenesis as compared with those implanted in wild-type mice. Injection of VEGF-neutralizing antibody but not the isotype-matched control antibody decreased endothelial-cell angiogenesis and tumor growth in vivo. Furthermore, LKB1 deletion enhanced mouse retinal and cell angiogenesis, and knockdown of VEGF by small-interfering RNA decreased endothelial cell proliferation and migration. Re-expression of LKB1 or knockdown of VEGF receptor 2 decreased the overproliferation and -migration observed in LKB1(endo-/-) cells. Mechanistically, LKB1 could bind to the VEGF transcription factor, specificity protein 1 (Sp1), which then inhibited the binding of Sp1 to the VEGF promoter to reduce VEGF expression. Endothelial LKB1 may regulate endothelial angiogenesis and tumor growth by modulating Sp1-mediated VEGF expression."}

{"project":"LitCoin-MONDO_bioort2019","denotations":[{"id":"T1","span":{"begin":81,"end":86},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T2","span":{"begin":264,"end":286},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T3","span":{"begin":292,"end":297},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T4","span":{"begin":367,"end":372},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T5","span":{"begin":826,"end":832},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T6","span":{"begin":1174,"end":1179},"obj":"DiseaseOrPhenotypicFeature"},{"id":"T7","span":{"begin":1749,"end":1754},"obj":"DiseaseOrPhenotypicFeature"}],"attributes":[{"id":"A2","pred":"#label","subj":"T2","obj":"D010580"},{"id":"A6","pred":"#label","subj":"T6","obj":"D009369"},{"id":"A4","pred":"#label","subj":"T4","obj":"D009369"},{"id":"A5","pred":"#label","subj":"T5","obj":"D009369"},{"id":"A1","pred":"#label","subj":"T1","obj":"D009369"},{"id":"A3","pred":"#label","subj":"T3","obj":"D009369"},{"id":"A7","pred":"#label","subj":"T7","obj":"D009369"}],"text":"Deletion of endothelial cell-specific liver kinase B1 increases angiogenesis and tumor growth via vascular endothelial growth factor.\nLiver kinase B1 (LKB1) is a serine/threonine protein kinase ubiquitously expressed in mammalian cells. It was first identified in Peutz-Jeghers syndrome as a tumor suppressor gene. Whether endothelial LKB1 regulates angiogenesis and tumor growth is unknown. In this study, we generated endothelial cell-specific LKB1-knockout (LKB1(endo-/-)) mice by crossbreeding vascular endothelial-cadherin-Cre mice with LKB1(flox/flox) mice. Vascular endothelial growth factor (VEGF) level was highly co-stained in endothelial cells but not in macrophages in LKB1(endo-/-) mice. Consistently, LKB1(endo-/-) mouse tissues including the lung, skin, kidney and liver showed increased vascular permeability. Tumors implanted in LKB1(endo-/-) mice but not macrophage-specific LKB1-knockout mice grew faster and showed enhanced vascular permeability and increased angiogenesis as compared with those implanted in wild-type mice. Injection of VEGF-neutralizing antibody but not the isotype-matched control antibody decreased endothelial-cell angiogenesis and tumor growth in vivo. Furthermore, LKB1 deletion enhanced mouse retinal and cell angiogenesis, and knockdown of VEGF by small-interfering RNA decreased endothelial cell proliferation and migration. Re-expression of LKB1 or knockdown of VEGF receptor 2 decreased the overproliferation and -migration observed in LKB1(endo-/-) cells. Mechanistically, LKB1 could bind to the VEGF transcription factor, specificity protein 1 (Sp1), which then inhibited the binding of Sp1 to the VEGF promoter to reduce VEGF expression. Endothelial LKB1 may regulate endothelial angiogenesis and tumor growth by modulating Sp1-mediated VEGF expression."}

{"project":"LitCoin-Chemical-MeSH-CHEBI","denotations":[{"id":"T1","span":{"begin":162,"end":168},"obj":"ChemicalEntity"},{"id":"T2","span":{"begin":169,"end":178},"obj":"ChemicalEntity"},{"id":"T3","span":{"begin":498,"end":527},"obj":"ChemicalEntity"},{"id":"T4","span":{"begin":1238,"end":1245},"obj":"ChemicalEntity"}],"attributes":[{"id":"A1","pred":"ID:","subj":"T1","obj":"http://purl.obolibrary.org/obo/CHEBI_17822"},{"id":"A2","pred":"ID:","subj":"T2","obj":"http://purl.obolibrary.org/obo/CHEBI_26986"},{"id":"A3","pred":"ID:","subj":"T3","obj":"C094954"},{"id":"A4","pred":"ID:","subj":"T4","obj":"D012172"},{"id":"A5","pred":"ID:","subj":"T4","obj":"http://purl.obolibrary.org/obo/CHEBI_15035"}],"text":"Deletion of endothelial cell-specific liver kinase B1 increases angiogenesis and tumor growth via vascular endothelial growth factor.\nLiver kinase B1 (LKB1) is a serine/threonine protein kinase ubiquitously expressed in mammalian cells. It was first identified in Peutz-Jeghers syndrome as a tumor suppressor gene. Whether endothelial LKB1 regulates angiogenesis and tumor growth is unknown. In this study, we generated endothelial cell-specific LKB1-knockout (LKB1(endo-/-)) mice by crossbreeding vascular endothelial-cadherin-Cre mice with LKB1(flox/flox) mice. Vascular endothelial growth factor (VEGF) level was highly co-stained in endothelial cells but not in macrophages in LKB1(endo-/-) mice. Consistently, LKB1(endo-/-) mouse tissues including the lung, skin, kidney and liver showed increased vascular permeability. Tumors implanted in LKB1(endo-/-) mice but not macrophage-specific LKB1-knockout mice grew faster and showed enhanced vascular permeability and increased angiogenesis as compared with those implanted in wild-type mice. Injection of VEGF-neutralizing antibody but not the isotype-matched control antibody decreased endothelial-cell angiogenesis and tumor growth in vivo. Furthermore, LKB1 deletion enhanced mouse retinal and cell angiogenesis, and knockdown of VEGF by small-interfering RNA decreased endothelial cell proliferation and migration. Re-expression of LKB1 or knockdown of VEGF receptor 2 decreased the overproliferation and -migration observed in LKB1(endo-/-) cells. Mechanistically, LKB1 could bind to the VEGF transcription factor, specificity protein 1 (Sp1), which then inhibited the binding of Sp1 to the VEGF promoter to reduce VEGF expression. Endothelial LKB1 may regulate endothelial angiogenesis and tumor growth by modulating Sp1-mediated VEGF expression."}

{"project":"LitCoin-NCBITaxon-2","denotations":[{"id":"T1","span":{"begin":476,"end":480},"obj":"OrganismTaxon"},{"id":"T2","span":{"begin":532,"end":536},"obj":"OrganismTaxon"},{"id":"T3","span":{"begin":558,"end":562},"obj":"OrganismTaxon"},{"id":"T4","span":{"begin":695,"end":699},"obj":"OrganismTaxon"},{"id":"T5","span":{"begin":729,"end":734},"obj":"OrganismTaxon"},{"id":"T6","span":{"begin":860,"end":864},"obj":"OrganismTaxon"},{"id":"T7","span":{"begin":907,"end":911},"obj":"OrganismTaxon"},{"id":"T8","span":{"begin":1039,"end":1043},"obj":"OrganismTaxon"},{"id":"T9","span":{"begin":1232,"end":1237},"obj":"OrganismTaxon"}],"text":"Deletion of endothelial cell-specific liver kinase B1 increases angiogenesis and tumor growth via vascular endothelial growth factor.\nLiver kinase B1 (LKB1) is a serine/threonine protein kinase ubiquitously expressed in mammalian cells. It was first identified in Peutz-Jeghers syndrome as a tumor suppressor gene. Whether endothelial LKB1 regulates angiogenesis and tumor growth is unknown. In this study, we generated endothelial cell-specific LKB1-knockout (LKB1(endo-/-)) mice by crossbreeding vascular endothelial-cadherin-Cre mice with LKB1(flox/flox) mice. Vascular endothelial growth factor (VEGF) level was highly co-stained in endothelial cells but not in macrophages in LKB1(endo-/-) mice. Consistently, LKB1(endo-/-) mouse tissues including the lung, skin, kidney and liver showed increased vascular permeability. Tumors implanted in LKB1(endo-/-) mice but not macrophage-specific LKB1-knockout mice grew faster and showed enhanced vascular permeability and increased angiogenesis as compared with those implanted in wild-type mice. Injection of VEGF-neutralizing antibody but not the isotype-matched control antibody decreased endothelial-cell angiogenesis and tumor growth in vivo. Furthermore, LKB1 deletion enhanced mouse retinal and cell angiogenesis, and knockdown of VEGF by small-interfering RNA decreased endothelial cell proliferation and migration. Re-expression of LKB1 or knockdown of VEGF receptor 2 decreased the overproliferation and -migration observed in LKB1(endo-/-) cells. Mechanistically, LKB1 could bind to the VEGF transcription factor, specificity protein 1 (Sp1), which then inhibited the binding of Sp1 to the VEGF promoter to reduce VEGF expression. Endothelial LKB1 may regulate endothelial angiogenesis and tumor growth by modulating Sp1-mediated VEGF expression."}

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of endothelial cell-specific liver kinase B1 increases angiogenesis and tumor growth via vascular endothelial growth factor.\nLiver kinase B1 (LKB1) is a serine/threonine protein kinase ubiquitously expressed in mammalian cells. It was first identified in Peutz-Jeghers syndrome as a tumor suppressor gene. Whether endothelial LKB1 regulates angiogenesis and tumor growth is unknown. In this study, we generated endothelial cell-specific LKB1-knockout (LKB1(endo-/-)) mice by crossbreeding vascular endothelial-cadherin-Cre mice with LKB1(flox/flox) mice. Vascular endothelial growth factor (VEGF) level was highly co-stained in endothelial cells but not in macrophages in LKB1(endo-/-) mice. Consistently, LKB1(endo-/-) mouse tissues including the lung, skin, kidney and liver showed increased vascular permeability. Tumors implanted in LKB1(endo-/-) mice but not macrophage-specific LKB1-knockout mice grew faster and showed enhanced vascular permeability and increased angiogenesis as compared with those implanted in wild-type mice. Injection of VEGF-neutralizing antibody but not the isotype-matched control antibody decreased endothelial-cell angiogenesis and tumor growth in vivo. Furthermore, LKB1 deletion enhanced mouse retinal and cell angiogenesis, and knockdown of VEGF by small-interfering RNA decreased endothelial cell proliferation and migration. Re-expression of LKB1 or knockdown of VEGF receptor 2 decreased the overproliferation and -migration observed in LKB1(endo-/-) cells. Mechanistically, LKB1 could bind to the VEGF transcription factor, specificity protein 1 (Sp1), which then inhibited the binding of Sp1 to the VEGF promoter to reduce VEGF expression. Endothelial LKB1 may regulate endothelial angiogenesis and tumor growth by modulating Sp1-mediated VEGF expression."}