Abstract
To analyze Pten and Smad4 gene expression in the urogenital system of Wistar rats in differents ages. Pten and Smad4 mRNA expression was assessed in the bladder, ventral prostate, testis, ovaries, and uterus by real-time PCR. Statistical analysis using the ANOVA (p<0.05). Pten levels showed a progressive age-dependent increase in the bladder (male and female) and prostate and were elevated in the ovaries of the middle-aged. In the uterus, no statistically significant differences were observed; in the testis, increased and decreased levels were seen in young adult and middle-aged rats, respectively. Smad4 expression was downregulated in the ovaries of the pubertal group but increased in the middle age group. In the uterus, Smad4 expression in the oldest group was higher than the others groups. In the testis, Smad4 expression steadily declined with age; in the prostate, it was higher in middle-aged rats than in younger rats. A similar trend was observed in the bladder of male and female middle-aged rats, compared with the pubertal group. The changes in phosphatase tensin homologue and Smad4 mRNA expression in Wistar rats appear to be associated with hormonal modifications in puberty and may be related to early follicular and testicular development.
Highlights
Cancer is the second most common cause of death worldwide
We evaluated the expression of the Pten and Smad[4] genes in the urogenital organs of Wistar rats at different ages
Pten mRNA expression in the bladder of middle-aged male rats was increased by 95%, 91%, and 80% relative to animals from the pre-pubertal, pubertal, and young adult groups, respectively (Table 2)
Summary
Cancer is the second most common cause of death worldwide. Breast, and colon cancers are the most commonly diagnosed cancers worldwide[1]. Multiple genes are related to the control of cellular proliferation and prevention of tumorigenesis. The Pten (phosphatase tensin homologue) gene encodes a protein phosphatase that functions as a tumor suppressor and is involved in various physiological processes, including cell proliferation, migration, survival, and apoptosis. Since its discovery in 1997, Pten has been established as one of the most commonly mutated tumor suppressors in human cancer; deficiency of Pten enzymatic activity has been implicated in the development of gliomas and breast, endometrial, lung, and prostate cancers[3]. The PTEN gene has been shown to be mutated in 40–50% of gliomas and in up to 70% of prostate cancers[4]
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