Correlation between the overexpression of epidermal growth factor receptor and mesenchymal makers in endometrial carcinoma / 부인종양

OBJECTIVE: The objective of this study was to evaluate the effect of overexpression of epidermal growth factor receptor (EGFR) on the expression of epithelial cell markers (E-cadherin and alpha-catenin) and mesenchymal cell markers (N-cadherin and vimentin) in endometrial carcinoma. METHODS: The expression of all 4 markers was evaluated in EGFR overexpressing Ishikawa cells, control Ishikawa cells, and KLE cells using reverse transcription polymerase chain reaction (RT-PCR) and Western blotting. The expression of these 4 markers was also determined in cancerous tissues of patients with endometrial carcinoma using immunohistochemical staining. RESULTS: Ishikawa cells transfected with EGFR showed decreased expression of E-cadherin and alpha-catenin and increased expression of N-cadherin and vimentin compared with control Ishikawa cells (p<0.01 for all). The expression of N-cadherin and vimentin was higher and the expression of E-cadherin and alpha-catenin was lower in stage II-III than stage I and in grade II-III than grade I endometrial carcinoma tissue (p<0.01 for all). CONCLUSION: Decreased expression of epithelial markers (E-cadherin and alpha-catenin) and increased expression of mesenchymal markers (N-cadherin and vimentin) were observed in human endometrial carcinoma tissue. These findings correlate with high EGFR expression in cultured endometrial carcinoma cells.

Expression of survivin in endometrial cancer and its role in regulating apoptosis of endometrial cancer cells / 肿瘤

Objective: To explore the expression of survivin in endometrial cancer and its roles in regulating apoptosis of endometrial cancer cells. Methods: Imnumohistochemistry was used to examine the expression of survivin in endometrial cancer specimens. RNA interference (RNAi) was applied to knock down survivin expression. The effect of RNAi was examined by RT-PCR and Western blotting. Cell apoptosis was detected by the FCM before and after RNAi. Western blotting was used to detect the expressions of caspase-3, caspase-8 and Bcl-2, which were closely associated with apoptosis. Results: The positive rate of survivin protein in endometrial cancer was obviously higher than those in atypical endometrium and normal endometrium (P < 0.05 and P < 0.01, respectively). RNAi effectively inhibited the expressions of survivin mRNA and survivin protein (P < 0.01). RNAi also induced cell apoptosis. Cell apoptosis rates in the two groups of RNAi were obviously higher than those in control groups (P < 0.01). Survivin RNAi also up-regulated the cleavage of caspase-3 and caspase-8. Conclusion: The aberrant expression of survivin may be closely related to the carcinogenesis of endometrial cancer, and inhibition of its expression may induce apoptosis of endometrial cancer cells.