The present invention relates to the prediction and treatment of cancers. In this study, the inventors analyzed how invalidation of the mitochondrial nucleoside diphosphate kinase (NDPK-D) functions affects the cellular behavior. HeLa cells, which naturally express low levels of NDPK-D, were stably transfected with expression vectors, either empty or designed to express NDPK-D wild type or mutant proteins. Single point mutations were chosen to suppress either the catalytic NDPK activity or its ability to bind the mitochondria inner membrane. Both loss-of-function mutations promoted altered mitochondrial structure and function, epithelial-mesenchymal transition and increased migratory and invasive potential. Immunocompromised mice developed more metastases when injected with cells expressing mutant NDPK-D as compared to wild-type. In human cancer, NME4 expression is negatively associated with tumor aggressiveness, and is a good prognosis factor for beneficial clinical outcome. Thus, the invention relates to a method for predicting the survival time of a patient suffering from a cancer comprising determining the expression level of NDPK-D and to the treatment of cancer in a subject in need thereof by using the NDPK-D protein or a fragment thereof or a fusion protein thereof and/or an agent for NDPK-D protein expression.