Vaughan Catherine, Pearsall Isabella, Yeudall Andrew, Deb Swati Palit, Deb Sumitra
Massey Cancer Center, Virginia Commonwealth University, 401 College Street, Richmond, VA, 23298, USA.
Subcell Biochem. 2014;85:71-90. doi: 10.1007/978-94-017-9211-0_4.
p53 is a tumor suppressor protein whose key function is to maintain the integrity of the cell. Mutations in p53 have been found in up to 50 % of all human cancers and cause an increase in oncogenic phenotypes such as proliferation and tumorigenicity. Both wild-type and mutant p53 have been shown to transactivate their target genes, either through directly binding to DNA, or indirectly through protein-protein interactions. This review discusses possible mechanisms behind both wild-type and mutant p53-mediated transactivation and touches on the concept of addiction to mutant p53 of cancer cells and how that may be used for future therapies.
p53是一种肿瘤抑制蛋白，其关键功能是维持细胞的完整性。在高达50%的人类癌症中都发现了p53的突变，这些突变会导致致癌表型增加，如增殖和致瘤性。野生型和突变型p53都已被证明可通过直接结合DNA或通过蛋白质-蛋白质相互作用间接激活其靶基因。本文综述了野生型和突变型p53介导的转录激活背后的可能机制，并探讨了癌细胞对突变型p53的依赖概念以及如何将其用于未来的治疗。
