Normally activation of p53 can result in cell cycle arrest, presumably to allow for DNA repair before replication or mitosis. In some cell types, however, p53 activation results in apoptosis as means of eliminating severely damaged cells. The final outcome of p53 activation depends on many factors, and is mediated largely through the action of downstream effector genes transactivated by p53.

p53 is shown to be either non-functional or mutated in most human cancers. The most common anomaly of p53 in human cancers is mutation of the p53 gene. Functional p53 provides a protective mechanism against tumor growth and a loss of p53 function is a key step in the neoplastic cascade. In addition, the function of p53 is critical to the success of many cancer treatments since radiation and chemotherapy act in part by triggering cell suicide in response to DNA damage. A successful response to therapy is greatly reduced in tumors where mutant p53 is present, and these tumors are often very difficult to treat.

BCL-2 is an anti-apoptotic protein located on the outer mitochondrial membrane. Anti-apoptotic members of the BCl-2 family are in the mitochondria and pro-apoptotic members are in the cytoplasm, but they translocate to mitochondrial upon receipt of apoptotic signals.

p53 levels are generally increased in cancer, yet the protein is likely non-functional or has reduced function. p53 levels increase because p53 mutants are no longer targeted by the Ubiquitin Ligase, Mdm2. Im not quite so sure about Bcl-2, but I think it too is often increased in cancer as Bcl-2 prevents apoptosis.

neither of them work independently, though higher bcl2 may have antiapoptotic

We are also doing work on DMBA induced cancer and DMH induced colon cancer..we had also analyzed the role of Bcl2 in the cancer chemoprevention.. Bcl2 acts as antiapoptotic and gets overexpressed in cancer. Therefore, it prevents apoptosis.

Great dear really helpful as other friends, thanks a lot

It is found that, In cancer cells, the oncogenic transcription factor STAT3 level is high. BCl-2 is a down-stream target of STAT3. Hence as we know, increase in STAT3 level automatically make an increase in BCl-2 level. BCl-2 protein is anti-apoptotic by its function.

About p53 level, I support the answer from Andrew Peak.

Great my prof thanks, its helpful

TP53 (tumor protein with MW ~53kDa) drew initial attentions from cancer community because its expression was high... it was initially thought as an oncogene.

About p53 protein, I completely agree with Andrew Paek.

J.Menezes.ITPAC,TOCANTINS

Normally activation of p53 can result in cell cycle arrest, presumably to allow for DNA repair before replication or mitosis. In some cell types, however, p53 activation results in apoptosis as means of eliminating severely damaged cells. The final outcome of p53 activation depends on many factors, and is mediated largely through the action of downstream effector genes transactivated by p53.

p53 is shown to be either non-functional or mutated in most human cancers. The most common anomaly of p53 in human cancers is mutation of the p53 gene. Functional p53 provides a protective mechanism against tumor growth and a loss of p53 function is a key step in the neoplastic cascade. In addition, the function of p53 is critical to the success of many cancer treatments since radiation and chemotherapy act in part by triggering cell suicide in response to DNA damage. A successful response to therapy is greatly reduced in tumors where mutant p53 is present, and these tumors are often very difficult to treat.

BCL-2 is an anti-apoptotic protein located on the outer mitochondrial membrane. Anti-apoptotic members of the BCl-2 family are in the mitochondria and pro-apoptotic members are in the cytoplasm, but they translocate to mitochondrial upon receipt of apoptotic signals.

More knowledge more great friends, thanks my Profs

The level of p53 expression is totally depends on the cell types. Example, SaoS2 and H1299 do not express p53; MDA-MB-468, SKBR3, and etc do express mutants p53 (Normally the level of p53 is higher compare to other cell lines as p53 mutants loss its ability to transactivate MDM2 to degrade itself), MCF7 express wild type p53.

The level of BCL-2 also depends on the cells type. As i know MDA-MB-468 does not express BCL-2. BCL-2 protein is belongs to antiapoptotic/pro-survival protein. Cheers~

p53 is tumor suppressor gene related to apoptosis as proapoptotic action BCL2 is antiapoptotic

p53 may increase or decrease according to the context i mean either normal or mutated.

P53 that up regulated in tumors is mutated form

Dear Gamal et al. Please see a brochure on p53 that you may like. I had written this a few years back, please ignore the prices etc. The scientific information is still good.

Thank you

Thanks dear friends for your too helpful information

Friends, I am giving a webinar on Angiogenesis: Its role in tumor growth and metastasis on May 24, 2012 at 9:30 am Pacific standard time (San Diego). If interested, here is the link to register and have access.

http://www.millipore.com/life_sciences/flx4/cancer_research_webinar

P53 is a regulator molecule , more influenced by redox and damaged degree of genome cells , as well she has a dynamic role at the cytoplasm and the nucleic compartment, it could be pro or anti proliferatif role linked to the phenotype of way cells