Study On Expression Of PTEN And Relationship With P-ERK In Prostate Cancer

[Objectives]: To identify the role of PTEN, Tumor Suppressor Gene in human prostate cancer, we detected the expression level of PTEN and evaluated its relationship with clinical pathological parameters and expression of P-ERK protein.[Methods]: Expression level of PTEN,P-ERK protein was examined in 47 prostate cancer and 9 prostate normal tissues by immunohistochemistry S-P method.[Results]: 1 .The positive rate of PTEN was significantly lower in prostate cancer (29.8%) than in normal tissues (88.9%, P<0.01). Expression level of PTEN protein decreased in C,D stage of prostate cancer compared to A,B stage of prostate cancer (P<0.01). The positive rate of PTEN oncoprotein was lower in poor differentiation tissues than in well differentiation tissues (P<0.05) and was lower in prostate cancer with lymphnode metastasis than in thoes without lymphnode metastasis (P<0.05).2.The positive rate of P-ERK was significantly higher in prostate cancer (93.3%) than in normal tissues (22.2%, P<0.01),expression level of p-ERK Was related to lymphnode metastasis and JWP stage(P<0.05).No correlation were found between expression level of P-ERK and histological differentiation(P>O.05)3.A significant negative relationship was observed between the expression of PTEN and P-ERK protein in prostate cancer (rs=-0.479, P<0.01).[Conclusions]: 1 .The abnormal expression of PTEN may play an important role in the development of prostate transitional cell carcinoma. PTEN examination might be useful for the judgement of tumor development and prognosis. 2. The hyperexpression of P-ERK may play an important role in the initiation and development of prostate cancer.3. PTEN and P-ERK can serve as a biomarker for prostate transitional cell carcinoma.4. The decrease or deletion of PTEN protein expression may not be able to effectively inhibit the over-activati-on of Ras/Raf/MEK/ERK signaling pathway,and this will result in abnormal proliferation and malignant transformation of hepatocytes in heptocellular carcinogenesis.