Re‐expression of p27 inhibits proliferation of endometrium cells from patients with endometriosis by modulating cell cycle‐related protein expression

Endometriosis is a benign gynaecologycal disease defined as the presence of functional endometrial implants out of uterus, mainly in pelvis. The cyclin‐dependent kinase inhibitor p27 kip1 seems to play a critical role in this process. Having this in mind, in the present study we investigated whether the re‐expression of p27 kip1 could modulate cell proliferative response in the endometrium of women with endometriosis. First generation bicistronic adenovirus: AdCMVhp27IRESEGFP (Adp27) and AdCMVNull (AdNull) were engineered. After transduction, the re‐expression of p27 kip1 was followed by a significant decrease in proliferation of endometrium cells obtained from women with endometriosis to a very close level of controls. In an attempt to better understand this anti‐proliferative effect, we also evaluate the expression of cell cycle‐related proteins (p16, p21, p27 and p53) in these cells. Results showed that p16, p21, p27 and p53 protein levels were markedly increased following Adp27 transduction. These findings further confirm our hypothesis that the lack of p27 expression in the topic endometrium of women with endometriosis might be one of the reasons that support proliferation of this tissue in places other than uterus. In addition, our results bring the interesting possibility for the use of Adp27 as a future strategy for the treatment of endometriosis.