The role of Cdc6 in cancer progression

CDC6 acts as a prototypical oncogenic stimulus operating in a bimodal manner (1-4): i) triggering replication stress, fueling genomic instability (1,2,3), ii) functioning as a transcriptional repressor by switching off the INK4A/ARF and CDH1 (E-cadherin) loci, disrupting cell cycle progression and cell-to-cell communication (3,4).

1) Karakaidos et al. Overexpression of the replication licensing regulators hCdt1 and hCdc6 characterizes a subset of non-small-cell lung carcinomas: synergistic effect with mutant p53 on tumor growth and chromosomal instability--evidence of E2F-1 transcriptional control over hCdt1. Am J Pathol 2004, 165(4): 1351-65.

2) Liontos et al. Deregulated overexpression of hCdt1 and hCdc6 promotes malignant behavior. Cancer Res 2007, 67(22): 10899-909.

3) Sideridou et al. Cdc6 expression represses E-cadherin transcription and activates adjacent replication origins. J Cell Biol 2011, 195(7): 1123-40.

4) Petrakis et al. Cdc6: a multi-functional molecular switch with critical role in carcinogenesis. Transcription 2012, 3(3): 124-9.

VG New

Prof. Vassilis G. Gorgoulis

Laboratory of Histology-Embryology
Molecular Carcinogenesis Group
Medical School
National and Kapodistrian University of Athens

 

Biomedical Research Foundation of the Academy of Athens

 

Faculty Institute for Cancer Sciences, University of Manchester,
Manchester Academic Health Science Centre, Manchester, UK

Manchester Centre for Cellular Metabolism,
University of Manchester, Manchester Academic Health Science Centre, Manchester

 

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