Z Li1, C-P Yu2, Y Zhong2, T-J Liu3, Q-D Huang4, X-H Zhao2, H Huang4, H Tu4, S Jiang2, Y Zhang2, J-H Liu5, L-B Song6. 1. Department of Experimental Research, State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-Sen University; Department of Gynecologic Oncology, the Third Affiliated Hospital of Kunming Medical College (Yunnan Tumor Hospital), Kunming, China. 2. Department of Experimental Research, State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-Sen University. 3. Guangzhou Laura Biotech Co., Ltd, Guangzhou. 4. Department of Gynecologic Oncology, Cancer Center, Sun Yat-Sen University. 5. Department of Gynecologic Oncology, Cancer Center, Sun Yat-Sen University. Electronic address: liujh@sysucc.org.cn. 6. Department of Experimental Research, State Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-Sen University. Electronic address: lb.song1@gmail.com.
Abstract
BACKGROUND: This study was aimed at investigating the role and molecular mechanism of Sam68 in cervical cancer lymph node metastasis. MATERIALS AND METHODS: Sam68 expression profile was detected by quantitative polymerase chain reaction, western blotting and immunohistochemical staining. Short hairpin RNA interfering approach was employed to suppress endogenous Sam68 expression in cervical cancer cells to determine its role in metastasis and the possible mechanism. RESULTS: Sam68 expression in cervical cancer was significantly up-regulated at both messenger RNA and protein levels compared with that in normal cervical tissues. The high expression level of Sam68 and its cytoplasmic localization were significantly associated with risk factors including pelvic lymph node metastasis (P < 0.001), and served as independent prognostic factors for predicting shortening of the overall survival time and disease-free survival time in patients with early-stage cervical cancer. Moreover, down-regulation of Sam68 in cervical cancer cells remarkably inhibited cellular motility and invasion. In addition, down-regulation of Sam68 reversed epithelial-mesenchymal transition through inhibiting the Akt/ GSK-3β/Snail pathway. CONCLUSION: This study demonstrated that Sam68 could induce cervical cancer lymph node metastasis through regulating epithelial-mesenchymal transition, and Sam68 expression profile possessed the potential to serve as predictors of pelvic lymph node metastasis in cervical cancer patients.
BACKGROUND: This study was aimed at investigating the role and molecular mechanism of Sam68 in cervical cancer lymph node metastasis. MATERIALS AND METHODS:Sam68 expression profile was detected by quantitative polymerase chain reaction, western blotting and immunohistochemical staining. Short hairpin RNA interfering approach was employed to suppress endogenous Sam68 expression in cervical cancer cells to determine its role in metastasis and the possible mechanism. RESULTS:Sam68 expression in cervical cancer was significantly up-regulated at both messenger RNA and protein levels compared with that in normal cervical tissues. The high expression level of Sam68 and its cytoplasmic localization were significantly associated with risk factors including pelvic lymph node metastasis (P < 0.001), and served as independent prognostic factors for predicting shortening of the overall survival time and disease-free survival time in patients with early-stage cervical cancer. Moreover, down-regulation of Sam68 in cervical cancer cells remarkably inhibited cellular motility and invasion. In addition, down-regulation of Sam68 reversed epithelial-mesenchymal transition through inhibiting the Akt/ GSK-3β/Snail pathway. CONCLUSION: This study demonstrated that Sam68 could induce cervical cancer lymph node metastasis through regulating epithelial-mesenchymal transition, and Sam68 expression profile possessed the potential to serve as predictors of pelvic lymph node metastasis in cervical cancerpatients.
Authors: Luisa F Escobar-Hoyos; Jie Yang; Jiawen Zhu; Julie-Ann Cavallo; Haiyan Zhai; Stephanie Burke; Antonius Koller; Emily I Chen; Kenneth R Shroyer Journal: Mod Pathol Date: 2013-09-20 Impact factor: 7.842