Transcription profiling of mouse CD8-IGF1R 3T3 cells and 3T3 Vector control treated for 24 h with vehicle or IGF1R inhibitor A-928605 reveals reversal of oncogene transformation and suppression of tumor growth by the novel IGF1R kinase inhibitor A-928605.
Ontology highlight
ABSTRACT: The insulin-like growth factor (IGF) axis is an important signaling pathway in the growth and survival of many cell types and has been implicated in multiple aspects of cancer progression from tumorigenesis to metastasis. The multiple roles of IGF signaling in cancer suggest that selective inhibition of the pathway might yield clinically effective therapeutics. Here we describe A-928605, a novel small molecule inhibitor of the receptor tyrosine kinase responsible for IGF signal transduction. This small molecule is able to abrogate activation of the pathway as shown by effects on the target and downstream effectors and is shown to be effective at inhibiting the proliferation of an oncogene addicted tumor model cell line (CD8-IGF1R 3T3) both in vitro and in vivo. Experiment Overall Design: CD8-IGF1R 3T3 cells and 3T3 Vector control treated for 24 h with vehicle or IGF1R inhibitor A-928605, all with 3 replicates.
ORGANISM(S): Mus musculus
SUBMITTER: Paul Jung
PROVIDER: E-GEOD-14024 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
ACCESS DATA