Tumor hypoxic stress, cellular plasticity and RKIP

Hypoxic stress is key element during tumor evolution as it can induce cellular, molecular and biochemical changes within the tumor and its microenvironment. Moreover, phenotypic changes caused by hypoxic stress such as epithelial-mesenchymal transition (EMT) of carcinoma cells can confer proinvasive, prometastatic, anti-apoptotic as well as therapy resistance properties to the cells, in part through modulation of their cellular plasticity. The molecular networks regulating EMT are important to decrypt because they may deliver candidate targets to prevent such resistance and provide biomarkers helpful to assess such resistance. Here we review the current knowledge on the role of the RAF kinase inhibitor protein (RKIP) and it's molecular network in regulating EMT and cellular plasticity in cancer.