Boyang Chang1, Su Li2, Qianting He3, Zhonghua Liu3, Luodan Zhao3, Tingting Zhao3, Anxun Wang4. 1. State Key Laboratory of Oncology in Southern China, Sun Yat-sen University Cancer Center, 510060 Guangzhou, Guangdong, P.R. China; Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital, Sun Yat-Sen University, 510080 Guangzhou, Guangdong, P.R. China. 2. State Key Laboratory of Oncology in Southern China, Sun Yat-sen University Cancer Center, 510060 Guangzhou, Guangdong, P.R. China. 3. Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital, Sun Yat-Sen University, 510080 Guangzhou, Guangdong, P.R. China. 4. Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital, Sun Yat-Sen University, 510080 Guangzhou, Guangdong, P.R. China. Electronic address: anxunwang@yahoo.com.
Abstract
BACKGROUND: Bmi-1 had been found to involve in self renewal of stem cells and tumorigenesis in various malignancies. In this study, we investigated the role of Bmi-1 in the development of salivary adenoid cystic carcinoma (SACC). METHODS: At first, we confirmed that the deregulation of Bmi-1 was a frequent event in SACC; up-regulation of Bmi-1 was correlated with clinical stages, vital status and distant metastasis and associated with reduced overall survival and disease free survival. SACC-LM cells, higher migration and invasion abilities, elevated the expression of Bmi-1 protein, epithelial-mesenchymal transition (EMT) related proteins (Snail, Slug and Vimentin) and cancer stem cells (CSCs) related proteins (ABCG2, Notch, ALDH-1, Oct-4, Nanog and Epcam) compared to the SACC-83 cells (lower migration and invasion abilities). The migration and invasion abilities were inhibited in SACC-LM cells upon Bmi-1 knockdown. Meanwhile, Bmi-1 knockdown resulted in simultaneous loss of stem cell markers and EMT markers in SACC-LM cells. CONCLUSION: Our studies confirm that Bmi-1 deregulation plays an important role in the development of SACC and contributes to the migration and the invasion abilities of SACC, which is involved in EMT and CSCs. GENERAL SIGNIFICANCE: To our knowledge, this is the first study revealing that Bmi-1 deregulation is associated with enhanced migration, invasion and poor prognosis in salivary adenoid cystic carcinoma.
BACKGROUND:Bmi-1 had been found to involve in self renewal of stem cells and tumorigenesis in various malignancies. In this study, we investigated the role of Bmi-1 in the development of salivary adenoid cystic carcinoma (SACC). METHODS: At first, we confirmed that the deregulation of Bmi-1 was a frequent event in SACC; up-regulation of Bmi-1 was correlated with clinical stages, vital status and distant metastasis and associated with reduced overall survival and disease free survival. SACC-LM cells, higher migration and invasion abilities, elevated the expression of Bmi-1 protein, epithelial-mesenchymal transition (EMT) related proteins (Snail, Slug and Vimentin) and cancer stem cells (CSCs) related proteins (ABCG2, Notch, ALDH-1, Oct-4, Nanog and Epcam) compared to the SACC-83 cells (lower migration and invasion abilities). The migration and invasion abilities were inhibited in SACC-LM cells upon Bmi-1 knockdown. Meanwhile, Bmi-1 knockdown resulted in simultaneous loss of stem cell markers and EMT markers in SACC-LM cells. CONCLUSION: Our studies confirm that Bmi-1 deregulation plays an important role in the development of SACC and contributes to the migration and the invasion abilities of SACC, which is involved in EMT and CSCs. GENERAL SIGNIFICANCE: To our knowledge, this is the first study revealing that Bmi-1 deregulation is associated with enhanced migration, invasion and poor prognosis in salivary adenoid cystic carcinoma.