Abstract:

Objective To investigate the roles of phosphatidylinositol 3 kinase （PI3K） and phosphorylated Akt （P-Akt） in the pathogenesis of cervical squamous cell carcinoma and condyloma acuminatum. Methods Immunohistochemistry and Western blot were used to detect the expressions of PI3K and P-Akt in tissue specimens from the lesions of 30 cases of cervical squamous cell carcinoma, 30 cases of condyloma acuminatum and the prepuce of 15 normal human controls. The average optical density and gray scale values were calculated and analyzed by t test and F test respectively. Results The expressions of PI3K and P-Akt were observed in only the basal layer of the epidermis of control specimens, but in the whole epidermis of condyloma acuminatum tissue specimens. Cervical squamous cell carcinoma tissue specimens displayed a stronger expression of PI3K and P-Akt compared with the control and condyloma acuminatum tissue specimens. As immunohistochemistry revealed, the average absorbance value for PI3K and P-Akt was 0.28 ± 0.05 and 0.20 ± 0.07 respectively in cervical squamous cell carcinoma tissue specimens, 0.22 ± 0.04 and 0.17 ± 0.03 respectively in condyloma acuminatum tissue specimens, and 0.16 ± 0.04 and 0.10 ± 0.02 respectively in the control tissue specimens; significant differences were observed in the expressions of PI3K and P-Akt among the three groups of tissue specimens （F = 44.87, 20.64, respectively, both P < 0.01）. The results of Western blot were consistent with those of immunohistochemistry, and there was a significant difference in the gray scale value for PI3K and P-Akt between cervical squamous cell carcinoma, condyloma acuminatum and control tissue specimens （3.48 ± 0.48 vs. 1.99 ± 0.11 vs. 1.00 ± 0.03, F = 354.83, P < 0.01; 3.33 ± 0.26 vs. 1.96 ± 0.11 vs. 1.00 ± 0.03, F = 302.33, P < 0.01）. Conclusions The PI3K/Akt signaling pathway is abnormally activated in condyloma acuminatum and cervical squamous cell carcinoma, and human papilloma virus may cause the abnormal proliferation of infected epithelium likely by affecting the upregulated expression of PI3K/P-Akt.