scholarly journals Role of T helper 17 cytokines in the tumour immune inflammation response of patients with laryngeal squamous cell carcinoma

2017 ◽  
Vol 14 (1) ◽  
pp. 561-568 ◽  
Author(s):  
Wei-Jing Tang ◽  
Lei Tao ◽  
Li-Ming Lu ◽  
Di Tang ◽  
Xiao-Lin Shi
2020 ◽  
Vol Volume 13 ◽  
pp. 5709-5719
Author(s):  
Yang Guo ◽  
Qiang Huang ◽  
Juan Zheng ◽  
Chi-Yao Hsueh ◽  
Xiaohui Yuan ◽  
...  

2015 ◽  
Vol 126 (4) ◽  
pp. E148-E155 ◽  
Author(s):  
Antonio Greco ◽  
Armando De Virgilio ◽  
Maria Ida Rizzo ◽  
Fabio Pandolfi ◽  
Davide Rosati ◽  
...  

Head & Neck ◽  
2015 ◽  
Vol 38 (2) ◽  
pp. 260-266 ◽  
Author(s):  
Omer Faruk Karatas ◽  
Betul Yuceturk ◽  
Ilknur Suer ◽  
Mehmet Yilmaz ◽  
Harun Cansiz ◽  
...  

2019 ◽  
Vol 39 (1) ◽  
Author(s):  
Yuan Li ◽  
Chenjuan Tao ◽  
Lili Dai ◽  
Caixia Cui ◽  
Chaohui Chen ◽  
...  

AbstractIntroduction: Laryngeal squamous cell carcinoma (LSCC) is a highly aggressive malignant cancer, but the molecular mechanisms underlying its development and progression remain largely elusive. The purpose of the present study is to investigate the expression profile and functional role of microRNA-625 (miR-625) in LSCC.Materials and methods: LSCC tissues and adjacent normal tissues were collected from 86 LSCC patients. The expression levels of miR-625 and SOX4 mRNA in tissues and cells were detected by RT-qPCR analysis. The expression levels of SOX4 and EMT-related proteins were detected by western blot analysis. In vitro cell proliferation, migration, and invasion were detected by MTT assay, colony formation assay, wound healing assay, and transwell invasion assay, respectively. Dual-luciferase reporter assay was performed to verify the binding relationship between miR-625 and the 3′-UTR of SOX4.Results: The results demonstrated that miR-625 is significantly down-regulated in clinical LSCC tissues, and its low expression may be closely associated with unfavorable clinicopathological characteristics of LSCC patients. Overexpression of miR-625 significantly suppressed the proliferation, migration, invasion, and EMT of LSCC cells. Furthermore, SOX4 was validated as a direct target of miR-625 in LSCC cells, and rescue experiments suggested that restoration of SOX4 blocked the tumor suppressive role of miR-625 in LSCC cells.Conclusions: Taken together, these findings highlighted a critical role of miR-625 in the pathogenesis of LSCC, and restoration of miR-625 could be considered as a potential therapeutic strategy against this fatal disease.


2015 ◽  
Vol 67 (4) ◽  
pp. 491-500 ◽  
Author(s):  
Rocco Cappellesso ◽  
Gino Marioni ◽  
Marika Crescenzi ◽  
Luciano Giacomelli ◽  
Vincenza Guzzardo ◽  
...  

2013 ◽  
Vol 109 (1) ◽  
pp. 172-183 ◽  
Author(s):  
G Halec ◽  
D Holzinger ◽  
M Schmitt ◽  
C Flechtenmacher ◽  
G Dyckhoff ◽  
...  

2017 ◽  
Vol 33 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Xiaoxia Wang ◽  
Chun He ◽  
Chaohui Li ◽  
Benhong Ren ◽  
Qing Deng ◽  
...  

Background: Laryngeal squamous cell carcinoma (LSCC) has a poor prognosis due to recurrence and metastasis. IQ-domain GTPase-activating protein 1 (IQGAP1), a scaffold protein, plays an important role in tumorigenesis and malignant development. In this study, we aimed to explore the role of IQGAP1 in LSCC. Methods: Expression of IQGAP1 in human LSCC specimens was assessed by immunohistochemistry. We also evaluated the roles of IQGAP1 in cell proliferation, migration and invasion and epithelial-to-mesenchymal transition (EMT) in Hep-2 cells. Results: The expression of IQGAP1 protein was significantly up-regulated in LSCC tissues compared with normal laryngeal tissues (p = 0.002). Furthermore, the knockdown of IQGAP1 in Hep-2 cells inhibited cell growth, migration and invasion. Moreover, we found that IQGAP1 silencing reversed EMT. Conclusions: These results show for the first time that IQGAP1 is up-regulated in LSCC tissues and plays an important role in LSCC cell proliferation and invasiveness, which indicates that IQGAP1 could work as an oncogene and may serve as a promising molecular target for treatment of LSCC.


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