In order to investigate the role of the PTEN expression in
carcinogenesis and development 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 hyperplasia, 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 respectively. 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
endometrial hyperplasia. The level of PTEN expression in patients with
endometrial carcinoma was significantly 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 part in the
tumorigenesis and development of
endometrial carcinoma.