In anti-tumor treatments but the relevance of

In vitro cellular senescence, triggeredby activation of oncogenes has been involved in anti-tumor treatments but therelevance of senescence against tumorigenesis is yet to be verified. Prostatecancer involves the altercation of numerous tumor suppressor genes among which PTENand p53 are the most commonly mutated genes. Functionally different PTEN andp53 are mutually dependent as PTEN provides stability to p53 and in return PTENgets enhancement in its transcription from p53. This study provides theinsights about the relationship between these two tumor suppressors. For thisstudy, mutant mice (PTEN and Trp23 deletion in prostate) were developed andsignificance of cellular senescence at different conditions were studied byemploying numerous techniques such as Cre/loxPtechnique for prostate-specific inactivation study, histopathological analysisand magnetic resonance imaging(MRI) were used to study early and later effectsof inactivation of both suppressors respectively and primary mouse embryonic fibroblastwere used to investigate the basis of mutual relationship between the twosuppressors. Complete inactivation of PTEN resulted non-lethal invasive mouse prostatecancer after 4-6 months of latency whereas Trp53 inactivation neither developedany pathological changes in mouse prostate nor produced any tumors but it acceleratedthe progression of tumor initiated by the PTEN inactivation. Inactivation ofboth PTEN and p53 genesĀ  resulted lethal invasiveprostate cancer in the mice by the age of seven months.

Furthermore, acute PTENinactivation induced cellular senescence through p53-mediated cellular pathway bothin vivo and in vitro. Also, cellular senescence was detected in early-stage humanprostate cancer. The findings of this study provides the relevance of cellularsenescence in restriction of tumorigenesis in vivo.

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