A twist for survival and cancer progression.
A major obstacle to the expansion of abnormal cells with significant proliferative potential is the induction of programmed cell death. Consequently, oncogene-driven hyperproliferation must be associated with apoptosis inhibition to allow malignant outgrowth. The oncogenic cooperation of N-Myc and Twist-1 in the development of neuroblastoma, the most common and deadly solid tumour of childhood, perfectly illustrates such a process. N-Myc promotes cell proliferation, whereas Twist-1 counteracts its pro-apoptotic properties by knocking-down the ARF/p53 pathway. On the basis of numerous recent studies reporting its overexpression in a variety of human cancers, we discuss in this review the role of Twist-1 as a potent inhibitor of the cell safety programs engaged in response to an abnormal mitogenic activity.
Puisieux
A
A
INSERM U590 Centre Léon Bérard, Université Claude Bernard Lyon 1, 69373 Lyon Cedex 08, France. puiseux@lyon.fnclcc.fr
Valsesia-Wittmann
S
S
Ansieau
S
S
D017209:Apoptosis; D001943:Breast Neoplasms / Q000503:physiopathology*; D049109:Cell Proliferation; D018450:Disease Progression; D006801:Humans; D009362:Neoplasm Metastasis; D009447:Neuroblastoma / Q000503:physiopathology*; D009687:Nuclear Proteins; D016271:Proto-Oncogene Proteins c-myc / Q000502:physiology; D013534:Survival; D051879:Twist-Related Protein 1
D009687:Nuclear Proteins; D016271:Proto-Oncogene Proteins c-myc; C103173:TWIST1 protein, human; D051879:Twist-Related Protein 1