http://purl.uniprot.org/citations/28714514 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
http://purl.uniprot.org/citations/28714514 | http://www.w3.org/2000/01/rdf-schema#comment | "The development and acquisition of multiple drug resistance in cancer cells remain a major obstacle in the treatment of bladder cancer. Nuclear translocation of Y box binding-1 (YB-1), which is a member of a family of DNA-binding proteins that contain a cold shock domain, plays a significant role in the acquisition of drug resistance by upregulating expression of the multidrug resistance-1 (MDR-1) gene product, p-glycoprotein. The tumor suppressor protein p53 is thought to be essential for nuclear translocation of YB-1. We hypothesized that nuclear translocation of YB-1 might be associated with drug resistance of bladder cancer with an abnormality of the TP53 gene that results in a mutated p53 protein. To test this hypothesis, we analyzed the association of YB-1 with drug resistance of TP53-mutated bladder cancer, including immunohistochemical analysis of YB-1, p-glycoprotein and p53 in vivo as well as the function of YB-1 nuclear translocation and regulation of its translocation by p53 in vitro. Additionally, we examined the association between the nuclear translocation of YB-1 and gemcitabine, a major anticancer-drug for bladder cancer, in cancer cell lines. Nuclear expression of YB-1 was correlated with the expression of p-glycoprotein and p53 in bladder cancer cases (p<0.05). In vitro, both introduction of TP53 and gemcitabine induced nuclear translocation of YB-1. These data indicate that YB-1 translocates to the nucleus coordinately with p53 expression and is involved in gemcitabine resistance in bladder cancer. Nuclear expression of YB-1 is important for resistance to chemotherapy including gemcitabine in TP53-mutated bladder cancer."xsd:string |
http://purl.uniprot.org/citations/28714514 | http://purl.org/dc/terms/identifier | "doi:10.3892/ijo.2017.4031"xsd:string |
http://purl.uniprot.org/citations/28714514 | http://purl.uniprot.org/core/author | "Yamashita T."xsd:string |
http://purl.uniprot.org/citations/28714514 | http://purl.uniprot.org/core/author | "Higashi M."xsd:string |
http://purl.uniprot.org/citations/28714514 | http://purl.uniprot.org/core/author | "Morozumi M."xsd:string |
http://purl.uniprot.org/citations/28714514 | http://purl.uniprot.org/core/author | "Momose S."xsd:string |
http://purl.uniprot.org/citations/28714514 | http://purl.uniprot.org/core/author | "Tamaru J.I."xsd:string |
http://purl.uniprot.org/citations/28714514 | http://purl.uniprot.org/core/date | "2017"xsd:gYear |
http://purl.uniprot.org/citations/28714514 | http://purl.uniprot.org/core/name | "Int J Oncol"xsd:string |
http://purl.uniprot.org/citations/28714514 | http://purl.uniprot.org/core/pages | "579-586"xsd:string |
http://purl.uniprot.org/citations/28714514 | http://purl.uniprot.org/core/title | "Nuclear expression of Y box binding-1 is important for resistance to chemotherapy including gemcitabine in TP53-mutated bladder cancer."xsd:string |
http://purl.uniprot.org/citations/28714514 | http://purl.uniprot.org/core/volume | "51"xsd:string |
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