scholarly journals PRL ‐3 promotes migration and invasion and is associated with poor prognosis in salivary adenoid cystic carcinoma

2015 ◽  
Vol 45 (2) ◽  
pp. 111-118 ◽  
Author(s):  
Qian Dong ◽  
Xueqiang Ding ◽  
Boyang Chang ◽  
Haihe Wang ◽  
Anxun Wang
Keyword(s):  
Adenoid Cystic Carcinoma ◽  
Poor Prognosis ◽  
Migration And Invasion ◽  
Salivary Adenoid Cystic Carcinoma ◽  
Adenoid Cystic

scholarly journals Claudin-7 Inhibits Proliferation and Metastasis in Salivary Adenoid Cystic Carcinoma Through Wnt/β-Catenin Signaling

2020 ◽  
Vol 29 ◽  
pp. 096368972094358
Author(s):  
Huan Ji ◽  
Xu Ding ◽  
Wei Zhang ◽  
Yang Zheng ◽  
Hongming Du ◽  
...  
Keyword(s):  
Adenoid Cystic Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Tumor Formation ◽  
Biological Behavior ◽  
Migration And Invasion ◽  
Salivary Adenoid Cystic Carcinoma ◽  
Mesenchymal Transition ◽  
Adenoid Cystic ◽  
Proliferation And Metastasis ◽  
And Gender

The aim of this study was to investigate claudin-7 (CLDN7) expression in salivary adenoid cystic carcinoma (SACC) and its function in SACC cells. We determined CLDN7 expression in SACC tumors via immunohistochemistry and western blotting and evaluated the association between CLDN7 expression and clinicopathologic variables. Besides this, we constructed a stably transfected CLDN7 knockdown SACC-LM cell line via RNAi and assessed its biological behavior changes (cell viability, migration, and invasion). The correlation between CLDN7 and epithelial-mesenchymal transition (EMT) was analyzed. Additionally, a subcutaneous tumor formation model was used to assess SACC-LM cells tumorigenicity after the CLDN7 knockdown. In the present study, we found the CLDN7 expression of tumor group was lower than that in normal salivary glands and was significantly correlated with lymph node metastasis, recurrence, and gender. CLDN7 knockdown could add the proliferation and metastasis ability of SACC by regulating EMT through Wnt/β-catenin signaling pathway. In addition, CLDN7 knockdown in SACC promoted tumor growth in nude mice. CLDN7 inhibits cell proliferation and metastasis by inactivating the Wnt/β-catenin signaling in SACC. Thus, CLDN7 expression might be a useful marker to identify the potential for progression in SACC.

scholarly journals Inhibition of DEC2 is Necessary for Exiting Cell Dormancy in Salivary Adenoid Cystic Carcinoma 

2020 ◽  
Author(s):  
Xiao Yang ◽  
Jia-shun Wu ◽  
Mao Li ◽  
Wei-long Zhang ◽  
Xiao-lei Gao ◽  
...  
Keyword(s):  
Adenoid Cystic Carcinoma ◽  
Lung Metastasis ◽  
Tumor Dormancy ◽  
Migration And Invasion ◽  
Salivary Adenoid Cystic Carcinoma ◽  
Adenoid Cystic ◽  
Metastasis Model ◽  
Cell Dormancy

Abstract Background: Patients were prone to have poor prognosis once dormant tumor cells being reactivated. However, the molecular mechanism of tumor cell dormancy remains poorly understood. This study aimed to investigate the function of DEC2 in the dormancy of salivary adenoid cystic carcinoma (SACC) in vitro and vivo. Methods: The function of DEC2 in tumor dormancy of SACC was investigated in nude mice by establishing primary and lung metastasis model. Meanwhile, the interaction between hypoxia and SACC dormancy and the role of DEC2 were demonstrated through CoCl2 induced hypoxia–mimicking microenvironments. Furthermore, the expression of DEC2 was detected by immunohistochemical staining in primary SACC samples with and without recurrence. Results: In the primary SACC, DEC2 overexpression inhibited cell proliferation, increased cell population arrested in G0/G1 phase, and participated in dormancy regulation, which limited tumor growth. Intriguingly, in the model of lung metastasis, the level of DEC2 was reduced significantly and resulted in dormancy exit and growth resumption of SACC cells. Then, we found that DEC2 may associate with hyoxia in contributing to tumor dormancy, which might provide a possible cue to explain the different roles of DEC2 in primary and metastasis lesions. And overexpression of DEC2 induced dormancy and promoted migration and invasion through activating EMT program. Finally, DEC2 positive expression was shown to be significantly correlated with recurrence and dormancy of SACC patients. Conclusions: These findings provide a novel insight into the role of DEC2 gene in tumor dormancy and metastasis.

scholarly journals SOD2 deregulation enhances migration, invasion and has poor prognosis in salivary adenoid cystic carcinoma

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Boyang Chang ◽  
Hang Yang ◽  
Yuan Jiao ◽  
Kefeng Wang ◽  
Zhonghua Liu ◽  
...  
Keyword(s):  
Adenoid Cystic Carcinoma ◽  
Poor Prognosis ◽  
Salivary Adenoid Cystic Carcinoma ◽  
Adenoid Cystic

scholarly journals Extracellular Vesicles from Carcinoma-Associated Fibroblasts Promote Epithelial-Mesenchymal Transition of Salivary Adenoid Cystic Carcinoma via Interleukin-6

2022 ◽  
Author(s):  
Jing Kong ◽  
Yan Ran ◽  
Lei Zhu ◽  
Jiao Li ◽  
Xue Liu ◽  
...  
Keyword(s):  
Adenoid Cystic Carcinoma ◽  
Extracellular Vesicles ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Migration And Invasion ◽  
High Tendency ◽  
Salivary Adenoid Cystic Carcinoma ◽  
Mesenchymal Transition ◽  
Adenoid Cystic ◽  
Carcinoma Associated Fibroblasts

Abstract Carcinoma-associated fibroblasts (CAF) play a pivotal role in cancer progression. Salivary adenoid cystic carcinoma (SACC) has a high tendency to invade and metastasize. Understanding how CAF interact with SACC cells is essential to develop new targeting therapies for SACC. Extracellular vesicles (EVs) play important roles in intercellular communication. However, the role of CAF-derived EVs in SACC invasion remains poorly understood. In this study, we show that CAF EVs promote the migration and invasion abilities of SACC cells. The expression of biomarkers of epithelial-mesenchymal transition (EMT) was higher in SACC cells treated with CAF EVs treated with CAF EVs than in the negative controls, and high levels of IL-6 were detected in CAF and their EVs. Knockdown of IL-6 in CAF decreased invasive abilities and EMT biomarker expression in SACC cells induced by CAF EVs. CAF EV-associated IL6 promoted SACC EMT by activating JAK2/STAT3 signaling pathway. These findings suggest that targeting CAF-derived EVs may be an effective strategy for inhibiting SACC invasion.

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