Khanna, Böckelman, Hemmes, Junttila, Wiksten, Lundin, Junnila, Murphy, Evan, Haglund, Westermarck, Ristimäki: "MYC-dependent regulation and prognostic role of CIP2A in gastric cancer." in: Journal of the National Cancer Institute, Vol. 101, Issue 11, pp. 793-805, (2009) (PubMed).
CMyc is a proto-oncogene, which is overexpressed in a wide range of human cancers. Myc gene encodes a transcription factor that regulates a great number of genes through binding on Enhancer Box sequences (E-boxes) and recruiting histone acetyltransferase. It can also act as a transcriptional repressor. It regulates cell growth, apoptosis, differentiation and stem cell self-renewal. Previous studies on the phosphorylation of c-Myc have suggested functional association between phosphorylation at Thr58/Ser62 by glycogen synthase kinase 3, cyclin dependent kinase, ERK2 and C-Jun N terminal Kinase (JNK), cell proliferation and cell cycle regulation. Phosphorylation at Ser62 is required for Ras-induced stabilization and is prerequisite for phosphorylation at Thr58 for its degradation.