In inactivation neither resulted any pathological changes in mouse

In vitro cellular senescence, triggered
by activation of oncogenes has been involved in anti-tumor treatments but the
relevance of senescence against tumorigenesis is yet to be proved.

Prostate cancer
involves the altercation of numerous tumor suppressor genes among which PTEN and
p53 are the most commonly mutated genes. Though PTEN and p53 are functionally
different, they are mutually dependent as PTEN provides stability to p53 and in
return PTEN gets enhancement in its transcription from p53. This study provides
the insights about the relationship between these two tumor suppressors. For
the study of inactivation of these tumor suppressors, mutant mice (PTEN and
Trp23 deletion in prostate) were developed and significance of cellular senescence
at various conditions were studied by employing numerous techniques such as Cre/loxP technique for prostate-specific
inactivation study, histopathological analysis and magnetic resonance
imaging(MRI) were used to study early and later effects of inactivation of both
suppressors respectively and primary mouse embryonic fibroblast were used to investigate
the basis of mutual relationship between the two suppressors. Complete inactivation
of PTEN resulted non-lethal invasive mouse prostate cancer after 4-6 months of
latency whereas Trp53 inactivation neither resulted any pathological changes in
mouse prostate nor produce any tumors but it accelerates the progression of
tumor initiated by the PTEN inactivation. When PTEN and p53 both genes were
inactivated, invasive prostate cancer was found in mice by the age of ten weeks
and was lethal by the age of seven months. Furthermore, acute PTEN inactivation
induced cellular senescence through p53-mediated cellular pathway both in vivo and in vitro. Also, cellular senescence was detected in early-stage human
prostate cancer. The findings of this study provides the relevance of cellular
senescence in restriction of tumorigenesis in vivo.

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