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http://purl.uniprot.org/citations/25874490http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/25874490http://www.w3.org/2000/01/rdf-schema#comment"Success of chemotherapy is generally impaired by multidrug resistance, intrinsic resistance, or acquired resistance to functionally and structurally irrelevant drugs. Multidrug resistance emerges via distinct mechanisms: increased drug export, decreased drug internalization, dysfunctional apoptotic machinery, increased DNA damage repair, altered cell cycle regulation, and increased drug detoxification. Several reports demonstrated that multidrug resistance is a multifaceted problem such that multidrug resistance correlates with increased aggressiveness and metastatic potential. Here, we tested the involvement of protein kinase D2, a serine/threonine kinase that was previously implicated in proliferation, drug resistance, and motility in doxorubicin-resistant MCF7 (MCF7/DOX) cell line, which served as an in vitro model for drug resistance and invasiveness. We showed that basal level activity of protein kinase D2 (PKD2) was higher in MCF7/DOX cells than parental MCF7 cells. To elucidate the roles of PKD2 MCF7/DOX, PKD2 expression was reduced via small interfering RNA (siRNA)-mediated knockdown. Results showed that acquired resistance of MCF7/DOX to doxorubicin was not affected by PKD2 silencing, while motility of MCF7/DOX cells was reduced. The results implied that PKD2 silencing might inhibit migration of MCF7/DOX cells without affecting chemoresistance significantly."xsd:string
http://purl.uniprot.org/citations/25874490http://purl.org/dc/terms/identifier"doi:10.1007/s13277-015-3081-3"xsd:string
http://purl.uniprot.org/citations/25874490http://purl.uniprot.org/core/author"Alpsoy A."xsd:string
http://purl.uniprot.org/citations/25874490http://purl.uniprot.org/core/author"Gunduz U."xsd:string
http://purl.uniprot.org/citations/25874490http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25874490http://purl.uniprot.org/core/name"Tumour Biol"xsd:string
http://purl.uniprot.org/citations/25874490http://purl.uniprot.org/core/pages"4417-4426"xsd:string
http://purl.uniprot.org/citations/25874490http://purl.uniprot.org/core/title"Protein kinase D2 silencing reduced motility of doxorubicin-resistant MCF7 cells."xsd:string
http://purl.uniprot.org/citations/25874490http://purl.uniprot.org/core/volume"36"xsd:string
http://purl.uniprot.org/citations/25874490http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/25874490
http://purl.uniprot.org/citations/25874490http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/25874490
http://purl.uniprot.org/uniprot/#_A0JLT6-mappedCitation-25874490http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25874490
http://purl.uniprot.org/uniprot/#_B4E125-mappedCitation-25874490http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25874490
http://purl.uniprot.org/uniprot/#_Q9BZL6-mappedCitation-25874490http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25874490
http://purl.uniprot.org/uniprot/#_Q8N2H2-mappedCitation-25874490http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/25874490
http://purl.uniprot.org/uniprot/B4E125http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25874490
http://purl.uniprot.org/uniprot/A0JLT6http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25874490
http://purl.uniprot.org/uniprot/Q9BZL6http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25874490
http://purl.uniprot.org/uniprot/Q8N2H2http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/25874490