Clinicopathological significance of p27 kip1 expression in endometrial carcinoma

Objectives: Endometrial carcinoma originates from the endometrium and is one of the most common gynecological malignancies worldwide. With appropriate treatment, the 5-year survival rate for endometrial carcinoma is approximately 80%. Therefore, recent studies have focused on finding tumor-specific markers that can predict the biological behavior of endometrial carcinoma in relation to cell motility and invasion. Methods The expression of p27 kip1 gene between 130 endometrial carcinoma tissues and normal endometrial tissues were analyzed through immunohistochemistry. The endometrial carcinoma cell lines Ishikawa(ISK) were cultured, the p27 kip1 -saRNA expression vector was constructed, and the endometrial carcinoma cells interfering with the expression of p27 kip1 gene was also established. Western blotting and RT-PCR were employed to verify whether saRNA could up-regulate the expression of p27 kip1 gene. Additionally, the proliferation, migration and invasion capacities in cell line after activating with p27 kip1 was detected through CCK-8 and Transwell assay respectively. Furthermore, MMP2 and MMP9 were detected by ELISA and epithelial-mesenchymal transition (EMT) related proteins including E-cadherin, N-cadherin and Vimentin were assessed by Western blotting analysis. Results Compared with normal endometrial tissues, the p27 kip1 expression levels in endometrial carcinoma tissues were decreased remarkably. saRNAs transfection significantly up-regulated expressions in endometrial carcinoma cell lines. The proliferation, invasion and migration ability were inhibited considerably by p27 kip1 -saRNA compared with the control group. The expression of E-cadherin was increased while the expression of N-cadherin, Vimentin, MMP-2 and MMP-9 was decreased activated by the p27 kip1 -saRNA. Conclusions p27 kip1 could be used as a prognostic factor of endometrial carcinoma. Activating the expression of p27 kip1 in endometrial carcinoma cell line could effectively inhibit the proliferation, invasion and migration, and its mechanism is related to the inhibition of EMT. p27 kip1 is potential target for the treatment of endometrial carcinoma.