almost all these ways of abrogation of p53 have now been examined in the context of comparing identification and gene expression patterns of transcriptional targets in the cells in reaction to various cellular stresses including chemo or radiosensitization and not taking a look at the role of p53 by itself. For-all p53 inactivation studies done, it’s been observed that they have some or other inherent disadvantages. It is usually assumed that intracellular expression of E6 or any viral protein targeting p53 shows a true p53 null phenotype, the significant warning nevertheless exists that these oncoproteins bind and restrict the activity of several cellular proteins (-)-MK 801 besides p53. On the other hand use of dominant damaging mutants of p53 for understanding the value of wild type p53 may lead to erroneous conclusions due to not known increases of function as well as an ineffective reduced total of endogenous p53 function. The other modes of attenuation and abrogation of p53 function are either temporary or in non isogenic type systems or are regulated by extra cellular transmission. Hence, the variations in attenuation and abrogation of p53 function may notably change functional outcome. Additionally, all information regarding relationship between reduction and mutated p53 or any genetic and biochemical changes hasn’t been definitely established since these studies were centered on cyst biopsies and cell lines already lacking wild typ-e p53. In addition to all these, some more novel properties Endosymbiotic theory of p53 are actually emerging including activation of signal transduction pathways and whether p53 is involved with shooting of such pathways that originate at the degree of the cell membrane. Because delineation of the role that p53 might play in cells has been affected by the possible lack of appropriate type, there is a continuing requirement for genetically matched cell systems that specifically vary in p53 protein status. Taken together this report describes the characterization of MCF 7As53 cell Icotinib line based on breast carcinoma MCF 7 cells as an isogenic cell program poor only in p53 protein because of its antisense term. This model provides a valuable tool to delineate the role of p53 in breast cancers and to help in more systemic approach to decipher both up and downstream functions of p53 in a complex signaling system of cancer cells. 5 bromo, and sources of supplies were as follows: doxorubicin, methylthiazolyl tertrazolium, wortmannin, pifithrin alpha, methyl B cyclodextrin 4 chloro3 indolyl W D galactoside were purchased from Sigma, MO, USA. Doxorubicin was dissolved in sterile water to prepare a stock of 50 mM. MTT was reconstituted as 1 mg/ml in DMEM without phenol red. PFT, wortmannin, and X Gal were reconstituted in DMSO.