Quantitative Proteomics Identify the Possible Tumor Suppressive Role of Protease-Activated Receptor-4 in Esophageal Squamous Cell Carcinoma Cells

2018 ◽  
Vol 25 (3) ◽  
pp. 937-943 ◽  
Author(s):  
Ming Wang ◽  
Shuhong An ◽  
Diyi Wang ◽  
Haizhen Ji ◽  
Min Geng ◽  
...  
2019 ◽  
Vol 45 (2) ◽  
pp. e85
Author(s):  
L. Bognar ◽  
S. Bellyei ◽  
I. Hegedus ◽  
K. Gombos ◽  
O.P. Horvath ◽  
...  

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Chia-Chin Li ◽  
Chih-Yi Chen ◽  
Ying-Hsiang Chou ◽  
Chih-Jen Huang ◽  
Hsiu-Ying Ku ◽  
...  

Abstract Background The role of radiotherapy for cT4bNanyM0 esophageal squamous cell carcinoma (ESqCC) is relatively unclear, with both chemotherapy (C/T) alone and definitive concurrent chemoradiotherapy (dCCRT) being treatment options in the current guidelines. We aimed to compare the survival of dCCRT versus C/T for these patients via a population-based approach. Methods Eligible cT4b ESqCC patients diagnosed between 2011 and 2017 were identified via the Taiwan Cancer Registry. We used propensity score (PS) weighting to balance the observable potential confounders between groups. The hazard ratio (HR) of death and incidence of esophageal cancer mortality (IECM) were compared between dCCRT and C/T. We also evaluated OS in subgroups of either low or standard radiotherapy doses. Results Our primary analysis consisted of 247 patients in whom covariates were well balanced after PS weighing. The HR for death when dCCRT was compared with C/T was 0.36 (95% confidence interval 0.24–0.53, P < 0.001). Similar results were found for IECM. Statistical significance was only observed in the standard RT dose but not in the low dose in subgroup analyses. Conclusions In this population-based nonrandomized study of cT4bNanyM0 ESqCC patients from Asia (Taiwan), we found that the use of radiotherapy with chemotherapy was associated with better overall survival than chemotherapy alone. Further studies (especially RCTs) are needed to confirm our findings.


2017 ◽  
Vol 23 ◽  
pp. 2382-2390 ◽  
Author(s):  
Lei Wang ◽  
Haiping Zhang ◽  
Ayshamgul Hasim ◽  
Abuduaini Tuerhong ◽  
Zhichao Hou ◽  
...  

2014 ◽  
Vol 127 (17) ◽  
pp. 3735-3744 ◽  
Author(s):  
J. Li ◽  
F. Shan ◽  
G. Xiong ◽  
X. Chen ◽  
X. Guan ◽  
...  

2016 ◽  
Vol 242 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Guanghui Cui ◽  
Donglei Liu ◽  
Weihao Li ◽  
Yuhang Li ◽  
Youguang Liang ◽  
...  

Increasing evidence suggests that miR-194 is down-regulated in esophageal squamous cell carcinoma tumor tissue. However, the role and underlying mechanism of miR-194 in esophageal squamous cell carcinoma have not been well defined. We used DIANA, TargetScan and miRanda to perform target prediction analysis and found KDM5B is a potential target of miR-194. Based on these findings, we speculated that miR-194 might play a role in esophageal squamous cell carcinoma development and progression by regulation the expression of KDM5B. We detected the expression of miR-194 and KDM5B by quantitative real-time reverse transcription PCR (qRT-PCR) and Western blot assays, respectively, and found down-regulation of miR-194 and up-regulation of KDM5B existed in esophageal squamous cell carcinoma cell lines. By detecting proliferation, invasion and apoptosis of TE6 and TE14 cells transfected with miR-194 mimics or mimic control, miR-194 was found to inhibit proliferation and invasion and promote apoptosis of esophageal squamous cell carcinoma cells. miR-194 was further verified to regulate proliferation, apoptosis and invasion of esophageal squamous cell carcinoma cells by directly targeting KDM5B. Furthermore, animal studies were performed and showed that overexpression of miR-194 inhibited the growth of esophageal squamous cell carcinoma tumors in vivo. These results confirmed our speculation that miR-194 targets KDM5B to inhibit esophageal squamous cell carcinoma development and progression. These findings offer new clues for esophageal squamous cell carcinoma development and progression and novel potential therapeutic targets for esophageal squamous cell carcinoma.


Author(s):  
Yoshihisa Matsumoto ◽  
Atsushi Shiozaki ◽  
Toshiyuki Kosuga ◽  
Michihiro Kudou ◽  
Hiroki Shimizu ◽  
...  

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