PubMed:21772334 JSONTXT

{"project":"DisGeNET","denotations":[{"id":"T0","span":{"begin":14,"end":22},"obj":"gene:57214"},{"id":"T1","span":{"begin":84,"end":96},"obj":"disease:C0007102"},{"id":"T2","span":{"begin":14,"end":22},"obj":"gene:57214"},{"id":"T3","span":{"begin":84,"end":96},"obj":"disease:C0699790"},{"id":"T4","span":{"begin":120,"end":128},"obj":"gene:57214"},{"id":"T5","span":{"begin":164,"end":172},"obj":"disease:C0001430"},{"id":"T6","span":{"begin":378,"end":386},"obj":"gene:57214"},{"id":"T7","span":{"begin":691,"end":706},"obj":"disease:C0001418"},{"id":"T8","span":{"begin":814,"end":822},"obj":"gene:57214"},{"id":"T9","span":{"begin":866,"end":881},"obj":"disease:C0001418"},{"id":"T10","span":{"begin":814,"end":822},"obj":"gene:57214"},{"id":"T11","span":{"begin":901,"end":908},"obj":"disease:C0006826"}],"relations":[{"id":"R1","pred":"associated_with","subj":"T0","obj":"T1"},{"id":"R2","pred":"associated_with","subj":"T2","obj":"T3"},{"id":"R3","pred":"associated_with","subj":"T4","obj":"T5"},{"id":"R4","pred":"associated_with","subj":"T6","obj":"T7"},{"id":"R5","pred":"associated_with","subj":"T8","obj":"T9"},{"id":"R6","pred":"associated_with","subj":"T10","obj":"T11"}],"namespaces":[{"prefix":"gene","uri":"http://www.ncbi.nlm.nih.gov/gene/"},{"prefix":"disease","uri":"http://purl.bioontology.org/ontology/MEDLINEPLUS/"}],"text":"Repression of KIAA1199 attenuates Wnt-signalling and decreases the proliferation of colon cancer cells.\nBACKGROUND: The KIAA1199 transcript is upregulated in colon adenomas and downregulated upon β-catenin knockdown.\nMETHODS: Transcript profiling was performed on \u003e500 colon biopsies, methylation profiling data were compared with transcript data. Immunohistochemistry assessed KIAA1199 protein expression in 270 stage II/III tumours (\u003e3 years follow-up). The effects of stable KIAA1199 knockdown in SW480 cells (three different constructs) were studied using transcriptional profiling, proliferation and protein analysis.\nRESULTS: The KIAA1199 transcript was strongly upregulated in 95% of adenocarcinomas. Absent expression in normal mucosa correlated with KIAA1199 promotor methylation. Nuclear and cytoplasmic KIAA1199 protein expression was identified in colon adenocarcinomas and other types of cancers. A subpopulation of patients with tumours strongly expressing KIAA1199 in the nucleus showed a better outcome with regard to recurrence as lung or liver metastases. The KIAA1199 knockdown affected the cell cycle and the Wnt-signalling pathway. Reduced cellular proliferation and decreased KI67, phosphorylated retinoblastoma, β-catenin and ASCL2 protein expression supported these findings. Eighteen Wnt-signalling genes differentially expressed upon KIAA1199 knockdown correlated with the KIAA1199 expression profile in clinical specimens.\nCONCLUSION: The KIAA1199 knockdown attenuates the effects of the Wnt/β-catenin signalling and it may thus be regarded as a regulatory part of this pathway."}

{"project":"DisGeNET5_gene_disease","denotations":[{"id":"21772334-0#14#22#gene57214","span":{"begin":14,"end":22},"obj":"gene57214"},{"id":"21772334-0#84#96#diseaseC0007102","span":{"begin":84,"end":96},"obj":"diseaseC0007102"},{"id":"21772334-0#84#96#diseaseC0699790","span":{"begin":84,"end":96},"obj":"diseaseC0699790"},{"id":"21772334-1#4#12#gene57214","span":{"begin":120,"end":128},"obj":"gene57214"},{"id":"21772334-1#48#56#diseaseC0001430","span":{"begin":164,"end":172},"obj":"diseaseC0001430"},{"id":"21772334-7#24#32#gene57214","span":{"begin":814,"end":822},"obj":"gene57214"},{"id":"21772334-7#76#91#diseaseC0001418","span":{"begin":866,"end":881},"obj":"diseaseC0001418"},{"id":"21772334-8#61#69#gene57214","span":{"begin":971,"end":979},"obj":"gene57214"},{"id":"21772334-8#146#162#diseaseC0494165","span":{"begin":1056,"end":1072},"obj":"diseaseC0494165"}],"relations":[{"id":"14#22#gene5721484#96#diseaseC0007102","pred":"associated_with","subj":"21772334-0#14#22#gene57214","obj":"21772334-0#84#96#diseaseC0007102"},{"id":"14#22#gene5721484#96#diseaseC0699790","pred":"associated_with","subj":"21772334-0#14#22#gene57214","obj":"21772334-0#84#96#diseaseC0699790"},{"id":"4#12#gene5721448#56#diseaseC0001430","pred":"associated_with","subj":"21772334-1#4#12#gene57214","obj":"21772334-1#48#56#diseaseC0001430"},{"id":"24#32#gene5721476#91#diseaseC0001418","pred":"associated_with","subj":"21772334-7#24#32#gene57214","obj":"21772334-7#76#91#diseaseC0001418"},{"id":"61#69#gene57214146#162#diseaseC0494165","pred":"associated_with","subj":"21772334-8#61#69#gene57214","obj":"21772334-8#146#162#diseaseC0494165"}],"text":"Repression of KIAA1199 attenuates Wnt-signalling and decreases the proliferation of colon cancer cells.\nBACKGROUND: The KIAA1199 transcript is upregulated in colon adenomas and downregulated upon β-catenin knockdown.\nMETHODS: Transcript profiling was performed on \u003e500 colon biopsies, methylation profiling data were compared with transcript data. Immunohistochemistry assessed KIAA1199 protein expression in 270 stage II/III tumours (\u003e3 years follow-up). The effects of stable KIAA1199 knockdown in SW480 cells (three different constructs) were studied using transcriptional profiling, proliferation and protein analysis.\nRESULTS: The KIAA1199 transcript was strongly upregulated in 95% of adenocarcinomas. Absent expression in normal mucosa correlated with KIAA1199 promotor methylation. Nuclear and cytoplasmic KIAA1199 protein expression was identified in colon adenocarcinomas and other types of cancers. A subpopulation of patients with tumours strongly expressing KIAA1199 in the nucleus showed a better outcome with regard to recurrence as lung or liver metastases. The KIAA1199 knockdown affected the cell cycle and the Wnt-signalling pathway. Reduced cellular proliferation and decreased KI67, phosphorylated retinoblastoma, β-catenin and ASCL2 protein expression supported these findings. Eighteen Wnt-signalling genes differentially expressed upon KIAA1199 knockdown correlated with the KIAA1199 expression profile in clinical specimens.\nCONCLUSION: The KIAA1199 knockdown attenuates the effects of the Wnt/β-catenin signalling and it may thus be regarded as a regulatory part of this pathway."}