In non-small cell lung cancer cells that contain a mutated KRAS gene, SIVA, a p53 target gene that is critical for apoptosis, is overexpressed in a p53-independent manner and promotes tumorigenesis through the stimulation of mTOR signaling. The ablation of Siva in conditional knockout mice results in an inhibition of tumor development that makes SIVA an interesting new candidate therapeutic target for the treatment of a carcinoma with few therapeutic options.
©2015 American Association for Cancer Research.