Mutant p53 Located in the Cytoplasm Inhibits Autophagy

摘要: Abstract The tumor suppressor protein p53 is a transcriptor factor highly mutated in cancer. In the last decades, research has demonstrated that, addition to its role nucleus, extranuclear functions regulation of cellular metabolism, oxidative stress, and drug response. Specifically, been shown have dual autophagy, mechanism that allows turnover old damaged proteins organelles, as well key cancer development. Nuclear increases autophagy; however, current indicates cytosolic p53, either wild-type or form, regulates autophagic pathway independently manner opposite from nuclear p53. this chapter, we discuss what known about pathways induced by mutants autophagy their impact on tumorigenesis. Knowledge signaling involved cytosolic-nuclear interplay will help identification targets might be used for development new therapies.