Abstract:
:This study aims to examine the expression of p53, p16, and murine double minute 2 (MDM2) protein in normal endometrium and endometriosis, in order to discuss the role of p53, p16, and MDM2 protein and apoptosis in the pathogenesis and development of endometriosis, and provide a theoretical basis for clinical diagnosis and treatment.The immunohistochemical streptavidin-biotin peroxidase method was used to detect the expression of p53, p16, and MDM2 in tissue samples obtained from 30 women with pathologically confirmed ovarian endometriosis and 29 women with pathologically confirmed normal endometrium. The relationship between p53, p16, and MDM2 expression and apoptosis was analyzed.In normal endometrium, the positive rate of p53 in the secretory phase was higher than that in the proliferative phase (P < .05). Furthermore, the positive rate of p53 in normal endometrium was higher than that in ovarian endometriosis (P < .05). There was a significant difference between normal endometrium and ovarian endometriosis.The positive rate of p16 in normal endometrium was higher than that in ovarian endometriosis (P < .05). Furthermore, there was a significant difference between normal endometrium and ovarian endometriosis. The positive rate of MDM2 in normal endometrium was lower than that in ovarian endometriosis (P < .05).In ovarian endometriosis, the expression of p53 and p16 was positively correlated with each other (r = 0.611, P < .01). However, the expression of p53 and MDM2 was negatively correlated with each other (r = -0.541, P < .01). Furthermore, the expression of p16 and MDM2 might not be relevant in the endometriosis (r = 0.404, P > .05).As important apoptosis regulatory genes, p53, p16, and MDM2 might be involved in the pathogenesis and development of endometriosis.
journal_name
Medicine (Baltimore)journal_title
Medicineauthors
Sang L,Fang QJ,Zhao XBdoi
10.1097/MD.0000000000014776subject
Has Abstractpub_date
2019-04-01 00:00:00pages
e14776issue
14eissn
0025-7974issn
1536-5964pii
00005792-201904050-00002journal_volume
98pub_type
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