Objective:To investigate the expression of PTEN in carcinogenesis and development of endometrial carcinoma.Methods:The expression of PTEN was detected by reverse transcription-polymerase chain reaction(RT-PCR)methods from 24 cases with endometrial carcinoma,10 cases with endometrial atypical hyperplasia,10 cases with endometrial hyperplasia and 10 cases with normal endometrium and by SP immunohistochemical methods from 73 cases with endometrial carcinoma,25 cases with endometrial atypical hyperplasia,71 cases with endometrial hyperplasia and 31 cases with normal endometrium.Results:PTEN expression of both RNA and protein in patients with endometrial carcinoma and endometrial atypical hyperplasia was significantly lower than that of patients with endometrial hyperplasia and normal endometrium.mRNA relative value was 0.35±0.13,0.46±0.11,2.32±0.32,2.45±0.51,respectively.Loss of PTEN expression rates were 66.67%(38/57),76.00%(19/25),5.63%(4/71),0(0/31),repectively.The results were also compared with clinical parameters.Loss of PTEN expression in patients with endometrial carcinoma was significantly related to histological classification(P<0.0001)and differentiation(P<0.05).It was not related to depth of myometrium invasion and clinical stage(P>0.05).Conclusion:Loss of PTEN expression is an early event in endometrial tumorigenesis.Detection of PTEN protein may be a diagnostic biomarker for endometrial precancers and adenocarcinoma.
Gao Qinglei Li Jing Xing Hui Lu Yunping Zhou Jianfeng Ma Ding
In order to investigate the role of the PTEN expression in carcinogenesis and develop-ment of endometrial carcinoma and clarify whether and how PTEN and PI3K/Akt pathway relate to endometrial carcinoma, the expression of PTEN and phospho-Akt was detected by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) methods and Western-blot from 24 cases of endometrial carcinoma, 10 cases of endometrial atypical hyperplasia, 10 cases of endometrial hy-perplasia, and 10 cases of normal endometrium. SP immunohistochemical methods were used to measure levels of PTEN protein expression in following 5 study groups: 31 cases of endometrium in proliferative phase, 30 cases of endometrium in secretory phase, 71 cases of endometrial hyperplasia, 25 cases of atypical hyperplasia and 73 cases of endometrial carcinoma. Immunostaining score of PTEN was 3.39±0.15 in proliferative phase, 1.90±0.21 in secretory phase, 3.34±0.29 in endometrial hyperplasia, 0.62±0.11 in atypical hyperplasia, and 0.74±0.19 in endometrial carcinoma, respectively. PTEN mRNA relative value in normal endometrium, endometrial hyperplasia, endometrial atypical hyperplasia, and endometrial carcinoma was 2.45±0.51, 2.32±0.32, 0.46±0.11, and 0.35±0.13 respec-tively. The expression levels of PTEN mRNA and protein in patients with endometrial carcinoma and atypical hyperplasia were significantly lower than in those of proliferative phase and with endo-metrial hyperplasia. The level of PTEN expression in patients with endometrial carcinoma was sig-nificantly related to tissue type (P<0.005), differentiation (P<0.05) and clinical stage (P<0.05), but not to depth of myometrium invasion (P>0.05). Western blot analysis revealed that Phospho-Akt level in PTEN negative cases was significantly higher, and there was a negative correlation between PTEN and phospho-Akt (r=-0.8973, P<0.0001). It was suggested that loss of PTEN expression was an early event in endometrial tumorigenesis. The phosphorylation of Akt induced by the loss of PTEN took par
