RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/22615908http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22615908http://www.w3.org/2000/01/rdf-schema#comment"

Background

AP-4 belongs to the basic helix-loop-helix leucine-zipper subgroup; it controls target gene expression, regulates growth, development and cell apoptosis and has been implicated in tumorigenesis. Our previous studies indicated that AP-4 was frequently overexpressed in gastric cancers and may be associated with the poor prognosis. The purpose of this study is to examine whether silencing of AP-4 can alter biological characteristics of gastric cancer cells.

Methods

Two specific siRNAs targeting AP-4 were designed, synthesized, and transfected into gastric cancer cell lines and human normal mucosa cells. AP-4 expression was measured with real-time quantitative PCR and Western blot. Cell proliferation and chemo-sensitivity were detected by CCK-8 assay. Cell cycle assay and apoptosis assay were performed by flow cytometer, and relative expression of cell cycle regulators were detected by real-time quantitative PCR and Western blot, expression of the factors involved in the apoptosis pathway were examined in mRNA and protein level.

Results

The expression of AP-4 was silenced by the siRNAs transfection and the effects of AP-4 knockdown lasted 24 to 96 hrs. The siRNA-mediated silencing of AP-4 suppressed the cellular proliferation, induced apoptosis and sensitized cancer cells to anticancer drugs. In addition, the expression level of p21, p53 and Caspase-9 were increased when AP-4 was knockdown, but the expression of cyclin D1, Bcl-2 and Bcl-x(L) was inhibited. It didn't induce cell cycle arrest when AP-4 was knockdown in p53 defect gastric cancer cell line Kato-III.

Conclusions

These results illustrated that gene silencing of AP-4 can efficiently inhibited cell proliferation, triggered apoptosis and sensitized cancer cells to anticancer drugs in vitro, suggesting that AP-4 siRNAs mediated silencing has a potential value in the treatment of human gastric cancer."xsd:string
http://purl.uniprot.org/citations/22615908http://purl.org/dc/terms/identifier"doi:10.1371/journal.pone.0037096"xsd:string
http://purl.uniprot.org/citations/22615908http://purl.uniprot.org/core/author"Chen J."xsd:string
http://purl.uniprot.org/citations/22615908http://purl.uniprot.org/core/author"Guo Y."xsd:string
http://purl.uniprot.org/citations/22615908http://purl.uniprot.org/core/author"Liu X."xsd:string
http://purl.uniprot.org/citations/22615908http://purl.uniprot.org/core/author"Liang Q."xsd:string
http://purl.uniprot.org/citations/22615908http://purl.uniprot.org/core/author"Wang G."xsd:string
http://purl.uniprot.org/citations/22615908http://purl.uniprot.org/core/author"Wu L."xsd:string
http://purl.uniprot.org/citations/22615908http://purl.uniprot.org/core/author"Zhang B."xsd:string
http://purl.uniprot.org/citations/22615908http://purl.uniprot.org/core/author"Wu C."xsd:string
http://purl.uniprot.org/citations/22615908http://purl.uniprot.org/core/author"Tao K."xsd:string
http://purl.uniprot.org/citations/22615908http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22615908http://purl.uniprot.org/core/name"PLoS One"xsd:string
http://purl.uniprot.org/citations/22615908http://purl.uniprot.org/core/pages"e37096"xsd:string
http://purl.uniprot.org/citations/22615908http://purl.uniprot.org/core/title"Down-regulation of AP-4 inhibits proliferation, induces cell cycle arrest and promotes apoptosis in human gastric cancer cells."xsd:string
http://purl.uniprot.org/citations/22615908http://purl.uniprot.org/core/volume"7"xsd:string
http://purl.uniprot.org/citations/22615908http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22615908
http://purl.uniprot.org/citations/22615908http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22615908
http://purl.uniprot.org/uniprot/#_Q01664-mappedCitation-22615908http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22615908
http://purl.uniprot.org/uniprot/#_Q59GG3-mappedCitation-22615908http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22615908
http://purl.uniprot.org/uniprot/#_Q6FHM5-mappedCitation-22615908http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/22615908
http://purl.uniprot.org/uniprot/Q6FHM5http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/22615908
http://purl.uniprot.org/uniprot/Q59GG3http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/22615908
http://purl.uniprot.org/uniprot/Q01664http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/22615908