Abstract

Heat shock protein of 72 kDa (HSP70) has a role in the functional modulation of sex steroid hormone receptors and in p53-associated oncogenesis and inhibits apoptosis associated with bcl-2. However, the exact role of HSP70 in the development of endometrial adenocarcinoma has not been well established. The aim of this study is to evaluate the role of HSP70 in relation with ER, PR, p53 and bcl-2 expressions and apoptosis in benign and malignant endometrial lesions. Immunohistochemical studies for HSP70, ER, PR, p53, bcl-2 and TUNEL method for apoptosis were performed in 30 cases of adenocarcinoma and 30 cases of benign endometrial lesions consisted of each 10 cases of disordered proliferative endometrium (DP), simple or complex hyperplasia (HP), and atypical hyperplasia (AH). There were no significant differences of HSP70 and bcl-2 expression rates and apoptotic index (AI) between DP, HP, AH, and adenocarcinoma. p53 expression rate in adenocarcinoma was 36.7%, but no p53 expression was identified in DP, HP and AH (p<0.05). In adenocarcinoma, HSP70 expression rate was higher in ER and PR negative adenocarcinoma (p<0.05), and p53 expression rate was higher in nonendometrioid type and FIGO grade II and III (p<0.05), but no significant difference of bcl-2 expression rate according to the histological type and FIGO grade. AI was higher in nonendometrioid type (p<0.05). There was no correlation between HSP70, p53 and bcl-2 expressions, and no significant difference of AI according to HSP70, ER, PR, p53, and bcl-2 expressions. In conclusion, higher HSP70 expression rate in poorly differentiated and ER and PR negative adenocarcinoma suggests that HSP70 inhibits ER and PR expression and may be involved in the development of poorly differentiated endometrial adenocarcinoma.

• Keywords: HSP70;Adenocarcinoma;Endometrium;