P16 and P21 are involved in the pathogenesis of endometrial thinning: A cross-sectional study.

P16 plays a role in the negative regulation of cell proliferation, regulating cell apoptosis to control the growth of tumor cells. P21 is a nuclear protein that suppresses DNA synthesis and inhibits cell division. This study aimed to examine the expression and roles of P16 and P21 in endometrial thinning. Thirty cases of endometrial biopsy diagnosed as endometrial thinning were assessed by p16 and p21 immunohistochemistry from March 2014 to August 2020 in Huazhong University of Science and Technology Union Shenzhen Hospital. Another thirty cases of normal endometrium in the same period were assessed as controls. The specimens underwent histological analysis, and P16 and P21 were assessed by immunohistochemistry. There were no statistically significant differences in age, menstrual cycle, BMI, sex hormone levels, gravidity and parity between the two groups (all P > .05). In the endometrial thinning group, P16 was expressed in the endometrial adenoid nucleus, cytolymph and interstitial cell nucleus. In the normal group, P16 was mainly expressed in the endometrial adenoid nucleus, with some P16 signals detected in the endometrial interstitial nucleus. P21 expression was mainly detected in the endometrial adenoid nucleus. P16 and P21 amounts in endometrial thinning cases were significantly lower than those of the normal endometrial group. There was no correlation between p16 and p21 amounts. This study revealed aberrant expression of P16 and P21 in the endometrium might be due to a compensatory effect of the thin endometrium to increase cell proliferation and suppress cell apoptosis. However, the pathological roles of P16 and P21 in endometrial thinning and the contribution of cell senescence deserve further investigation.