Dataset: Transcription profiling of human melanoma cells reveals KINK-1 a novel small-molecule inhibitor of IKK, enhances susceptibility of melanoma cells to antitumoral treatment

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-B-1), a highly selective small-molecule IKK inhibitor, as a potent suppressor of both constitutive and induced NF-B activity in melanoma cells. While KINK-1 profoundly diminished various NF-B-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-B activation, a mechanism implicated in chemoresistance, was abrogated by KINK-1. In addition, when KINK-1 was combined with doxorubicin in an in vivo melanoma model, experimental metastasis was significantly diminished as compared to either treatment alone. Induction of chemoresistance by KINK-1 in vivo was not observed. Thus, KINK-1 or related substances might increase the susceptibility of tumors to chemotherapy. Experiment Overall Design: one control and two time point (12hrs and 24hrs) are analyzed, with one replicate each (6 arrays total)

Species:

human

Samples:

6

Source:

E-GEOD-8772

Updated:

Dec.12, 2014

Registered:

Sep.22, 2014