Results

RDF/XMLNTriplesTurtleShow queryShare ▶
SubjectPredicateObject
http://purl.uniprot.org/citations/24811094http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24811094http://www.w3.org/2000/01/rdf-schema#comment"

Objective

Basic fibroblast growth factor (FGF2)-mediated Extracellular signal-regulated kinases1/2 (ERK1/2) signaling is a critical modulator in angiogenesis. SPRY4 has been reported to be a feedback negative regulator of FGFs-induced ERK1/2 signaling. The aim of this study was to explore the role of SPRY4 in endometrial adenocarcinoma cell.

Materials and methods

The effect of SPRY4 expression on FGF2-mediated ERK1/2 signaling was detected by luciferase assay and Western blot analysis. The growth of Ishikawa cells was detected using colony formation assay and cell number counting experiment.

Results

We found that plasmid-driven SPRY4 expression efficiently blocked the activity of FGF2-induced ERK1/2 signaling in Ishikawa cells. SPRY4 expression significantly reduced the proliferation and 17β-estradiol-induced proliferation of Ishikawa cells.

Conclusion

SPRY4 may function as a tumor suppressor in endometrial adenocarcinoma."xsd:string
http://purl.uniprot.org/citations/24811094http://purl.org/dc/terms/identifier"doi:10.3109/09513590.2014.912264"xsd:string
http://purl.uniprot.org/citations/24811094http://purl.uniprot.org/core/author"Li C."xsd:string
http://purl.uniprot.org/citations/24811094http://purl.uniprot.org/core/author"Li M."xsd:string
http://purl.uniprot.org/citations/24811094http://purl.uniprot.org/core/author"Wang C."xsd:string
http://purl.uniprot.org/citations/24811094http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/24811094http://purl.uniprot.org/core/author"Zhao X."xsd:string
http://purl.uniprot.org/citations/24811094http://purl.uniprot.org/core/author"Yan L."xsd:string
http://purl.uniprot.org/citations/24811094http://purl.uniprot.org/core/author"Li C.'"xsd:string
http://purl.uniprot.org/citations/24811094http://purl.uniprot.org/core/date"2014"xsd:gYear
http://purl.uniprot.org/citations/24811094http://purl.uniprot.org/core/name"Gynecol Endocrinol"xsd:string
http://purl.uniprot.org/citations/24811094http://purl.uniprot.org/core/pages"600-604"xsd:string
http://purl.uniprot.org/citations/24811094http://purl.uniprot.org/core/title"SPRY4-mediated ERK1/2 signaling inhibition abolishes 17beta-estradiol-induced cell growth in endometrial adenocarcinoma cell."xsd:string
http://purl.uniprot.org/citations/24811094http://purl.uniprot.org/core/volume"30"xsd:string
http://purl.uniprot.org/citations/24811094http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/24811094
http://purl.uniprot.org/citations/24811094http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/24811094
http://purl.uniprot.org/uniprot/#_A0A0C4DFS6-mappedCitation-24811094http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24811094
http://purl.uniprot.org/uniprot/#_A0A5P8KPE6-mappedCitation-24811094http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24811094
http://purl.uniprot.org/uniprot/#_Q9BXY1-mappedCitation-24811094http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24811094
http://purl.uniprot.org/uniprot/#_Q9C004-mappedCitation-24811094http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/24811094
http://purl.uniprot.org/uniprot/A0A5P8KPE6http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/24811094
http://purl.uniprot.org/uniprot/Q9C004http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/24811094
http://purl.uniprot.org/uniprot/Q9BXY1http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/24811094
http://purl.uniprot.org/uniprot/A0A0C4DFS6http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/24811094
▶