期刊
CELL DEATH AND DIFFERENTIATION
卷 18, 期 9, 页码 1487-1499出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2011.81
关键词
p63; p53; p73; cancer; metastasis; tumor suppressor
资金
- Medical Research Council, UK
- Istituto Superiore di Sanita 'Alleanza contro il Cancro' [ACC12]
- MIUR/PRIN
- MIUR/FIRB [RBIP06LCA9_0023]
- AIRC [5471]
- Italian Human ProteomeNet [RBRN07BMCT]
- Min Salute (Ricerca oncologica) [RF06, RF07]
- Telethon Melino [GGP09133]
- IDI-IRCCS
- MRC [MC_U132670600] Funding Source: UKRI
- Medical Research Council [MC_U132670600] Funding Source: researchfish
p53 mutations, occurring in two- thirds of all human cancers, confer a gain of function phenotype, including the ability to form metastasis, the determining feature in the prognosis of most human cancer. This effect seems mediated at least partially by its ability to physically interact with p63, thus affecting a cell invasion pathway, and accordingly, p63 is deregulated in human cancers. In addition, p63, as an 'epithelial organizer', directly impinges on epidermal mesenchimal transition, stemness, senescence, cell death and cell cycle arrest, all determinant in cancer, and thus p63 affects chemosensitivity and chemoresistance. This demonstrates an important role for p63 in cancer development and its progression, and the aim of this review is to set this new evidence that links p63 to metastasis within the context of the long conserved other functions of p63. Cell Death and Differentiation (2011) 18, 1487-1499; doi:10.1038/cdd.2011.81; published online 15 July 2011
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