{"database":"biostudies-other","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Schoen Margarete"],"species":["Homo sapiens"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-ECPF-GEOD-8772"],"project":["EurocanPlatform"],"abstract":["Interference with chemoresistance to enhance the efficacy of chemotherapeutics may be of great utility for cancer therapy. We have identified KINK-1 (Kinase Inhibitor of NF-κB-1), a highly selective small-molecule IKKβ inhibitor, as a potent suppressor of both constitutive and induced NF-κB activity in melanoma cells. While KINK-1 profoundly diminished various NF-κB-dependent gene products regulating proliferation, cytokine production or anti-apoptotic responses, the compound by itself showed little antiproliferative or pro-apoptotic activity on the cellular level. However, its combination with some cytostatics markedly enhanced their antitumoral activities in vitro, and doxorubicin-induced NF-κB activation, a mechanism implicated in chemoresistance, was abrogated by KINK-1. In addition, w"],"repository":["biostudies-other"],"experiment_type":["transcription profiling by array"],"data_source":["EurocanPlatform"],"pubmed_authors":["Schoen Margarete"],"additional_accession":[]},"is_claimable":false,"name":"Transcription profiling of human melanoma cells reveals KINK-1 a novel small-molecule inhibitor of IKK, enhances susceptibility of melanoma cells to antitumoral treatment","description":"Interference with chemoresistance to enhance the efficacy of chemotherapeutics may be of great utility for cancer therapy. We have identified KINK-1 (Kinase Inhibitor of NF-κB-1), a highly selective small-molecule IKKβ inhibitor, as a potent suppressor of both constitutive and induced NF-κB activity in melanoma cells. While KINK-1 profoundly diminished various NF-κB-dependent gene products regulating proliferation, cytokine production or anti-apoptotic responses, the compound by itself showed little antiproliferative or pro-apoptotic activity on the cellular level. However, its combination with some cytostatics markedly enhanced their antitumoral activities in vitro, and doxorubicin-induced NF-κB activation, a mechanism implicated in chemoresistance, was abrogated by KINK-1. In addition, w","dates":{"release":"2016-04-14T14:44:41Z","modification":"2016-04-14T14:44:41Z","creation":"2016-04-14T14:44:41Z"},"accession":"S-ECPF-GEOD-8772","cross_references":{"GEO":["GSE8772"],"ArrayExpress":["E-GEOD-8772"],"EFO":["EFO_0000756","EFO_0000322"],"ArrayExpress files":["E-GEOD-8772"]}}