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AuthorMarei H.E.
AuthorAlthani A.
AuthorAfifi N.
AuthorHasan, Anwarul
AuthorCaceci T.
AuthorPozzoli G.
AuthorMorrione A.
AuthorGiordano A.
AuthorCenciarelli C.
Available date2022-05-21T10:18:25Z
Publication Date2021
Publication NameCancer Cell International
ResourceScopus
Identifierhttp://dx.doi.org/10.1186/s12935-021-02396-8
URIhttp://hdl.handle.net/10576/31252
AbstractThe p53 protein is a transcription factor known as the "guardian of the genome" because of its critical function in preserving genomic integrity. The TP53 gene is mutated in approximately half of all human malignancies, including those of the breast, colon, lung, liver, prostate, bladder, and skin. When DNA damage occurs, the TP53 gene on human chromosome 17 stops the cell cycle. If p53 protein is mutated, the cell cycle is unrestricted and the damaged DNA is replicated, resulting in uncontrolled cell proliferation and cancer tumours. Tumor-associated p53 mutations are usually associated with phenotypes distinct from those caused by the loss of the tumor-suppressing function exerted by wild-type p53protein. Many of these mutant p53 proteins have oncogenic characteristics, and therefore modulate the ability of cancer cells to proliferate, escape apoptosis, invade and metastasize. Because p53 deficiency is so common in human cancer, this protein is an excellent option for cancer treatment. In this review, we will discuss some of the molecular pathways by which mutant p53 proteins might perform their oncogenic activities, as well as prospective treatment methods based on restoring tumor suppressive p53 functions
Languageen
PublisherBioMed Central Ltd
SubjectCancer progression
Cancer therapy
Gain of function mutation
p53 signaling
Tumor suppressor gene
Titlep53 signaling in cancer progression and therapy
TypeArticle
Pagination341-357
Issue Number1
Volume Number21
dc.accessType Abstract Only


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