scholarly journals The NOTCH1-HEY1 pathway regulates self-renewal and epithelial-mesenchymal transition of salivary adenoid cystic carcinoma cells

2020 ◽  
Vol 16 (4) ◽  
pp. 598-610 ◽  
Author(s):  
Jing Xie ◽  
Li-song Lin ◽  
Xiao-yu Huang ◽  
Rui-huan Gan ◽  
Lin-can Ding ◽  
...  
Keyword(s):  
Adenoid Cystic Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Carcinoma Cells ◽  
Self Renewal ◽  
Salivary Adenoid Cystic Carcinoma ◽  
Mesenchymal Transition ◽  
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 Thioredoxin 1 mediates TGF-β-induced epithelial-mesenchymal transition in salivary adenoid cystic carcinoma

Oncotarget ◽  
2015 ◽  
Vol 6 (28) ◽  
pp. 25506-25519 ◽  
Author(s):  
Yang Jiang ◽  
Xin Feng ◽  
Lei Zheng ◽  
Sheng-Lin Li ◽  
Xi-Yuan Ge ◽  
...  
Keyword(s):  
Adenoid Cystic Carcinoma ◽  
Epithelial Mesenchymal Transition ◽  
Salivary Adenoid Cystic Carcinoma ◽  
Mesenchymal Transition ◽  
Adenoid Cystic ◽  
Thioredoxin 1

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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