Cancer Science & Therapy

ISSN: 1948-5956

Open Access

A Mini Review on an Enigma of Mutant P53


Musadiq Ali*

There are many genes that have been explored in relation with cancer. But 50 percent of cancers occur due to mutation in P53. In the beginning, there was a thought that P53 act as an oncogenic protein instead of suppressing cancers. Now we have reached on conclusion that mutant P53 instead of wild type, act as an oncogenic protein. Through research carried out in the past, it has been concluded that gain of function mutation in the P53 has early onset of cancer as compared to mutant P53 with loss of function. A number of hotspots for mutation in P53 such as R175, G245, R248, R249, R273 and R282 have been identified in the past. Mutant P53 interact and inhibit proteins normal functioning such as p63, MRE11, Rad51-NSB complex, p73 and Sp-1. Mutant P53 also lead to enhance functioning of protein such as SREBP, NF-Y, VDR, ETS2 and NRF2. For proper folding of wild type P53 Zn+2 is necessary. There are microRNAs which are under the control of mutant P53. Mostly, PRIMA-1 analog has been used to reactivate the mutant P53 to wild type.


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