scholarly journals High expression of the long noncoding RNA SH3PXD2A-AS1 is associated with poor prognosis in patients with esophageal squamous cell carcinoma

2020 ◽  
Vol 48 (9) ◽  
pp. 030006052094905
Author(s):  
Qiuli Luo ◽  
Shanshan Wang ◽  
Haibo Han ◽  
Fei Xie ◽  
Jinfeng Chen

Objective Our objective was to explore the prognostic role of long noncoding RNA (lncRNA) SH3PXD2A-AS1 in esophageal squamous cell carcinoma (ESCC). Methods An SH3PXD2A-AS1 expression dataset was retrieved and analyzed from The Cancer Genome Atlas database, and SH3PXD2A-AS1 expression was determined in our cohort of 134 ESCC patients by using quantitative PCR. The clinical significance of SH3PXD2A-AS1 expression was investigated by the Chi square test and its prognostic value was determined by Kaplan–Meier survival curve analysis and Cox proportional hazards analysis. RNA interference and in vitro functional experiments, including cell viability, migration, and invasion, were used to investigate effects of SH3PXD2A-AS1 on cell malignant phenotype. Results SH3PXD2A-AS1 expression was increased in ESCC tissues compared with adjacent normal tissues. A high level of SH3PXD2A-AS1 expression was associated with poor tumor differentiation and advanced T, N, and TNM stages, indicating its oncogenic role in ESCC. Moreover, its high expression predicted poor overall survival in patients with ESCC. Inhibition of SH3PXD2A-AS1 expression significantly suppressed cell viability, migration, and invasion of ESCC cells. Conclusion High SH3PXD2A-AS1 expression is a poor prognostic factor for patients with ESCC. SH3PXD2A-AS1 might function as an oncogene that can promote malignant biological characteristics of ESCC cells.

Tumor Biology ◽  
2014 ◽  
Vol 35 (8) ◽  
pp. 7743-7754 ◽  
Author(s):  
Hai-Wei Xie ◽  
Qing-Quan Wu ◽  
Bin Zhu ◽  
Fang-Jun Chen ◽  
Lv Ji ◽  
...  

2018 ◽  
Vol 31 (Supplement_1) ◽  
pp. 179-179
Author(s):  
Toshiyuki Kobayashi ◽  
Atsushi Shiozaki ◽  
Hitoshi Fujiwara ◽  
Hirotaka Konishi ◽  
Yoshito Nako ◽  
...  

Abstract Background Recent studies have reported important roles for chloride intracellular channel 1 (CLIC1) in various cancers; however, its involvement in esophageal squamous cell carcinoma (ESCC) remains unclear. The aim of the present study was to investigate the role of CLIC1 in human ESCC. Methods CLIC1 expression in human ESCC cell lines was analyzed by Western blotting. Knockdown experiments were conducted with CLIC1 siRNA, and their effects on cell proliferation, the cell cycle, apoptosis, migration, and invasion were analyzed. The gene expression profiles of cells were analyzed using a microarray analysis. An immunohistochemical analysis was performed on 61 primary tumor samples obtained from ESCC patients who underwent esophagectomy. Results ESCC cells strongly expressed CLIC1. The depletion of CLIC1 using siRNA inhibited cell proliferation, induced apoptosis, and promoted cell migration and invasion. The results of the microarray analysis revealed that the depletion of CLIC1 regulated apoptosis via the TLR2/JNK pathway. Immunohistochemistry showed that CLIC1 was present in the cytoplasm of carcinoma cells, and that the very strong or very weak expression of CLIC1 was an independent poor prognostic factor. Conclusion The present results suggest that the very strong expression of CLIC1 enhances tumor survival, while its very weak expression promotes cellular movement. The present study provides an insight into the role of CLIC1 as a switch among tumor behaviors in ESCC. Disclosure All authors have declared no conflicts of interest.


2017 ◽  
Vol 32 (4) ◽  
pp. 403-408 ◽  
Author(s):  
Hongfen Liu ◽  
Qiang Zhen ◽  
Yakun Fan

Background Recent studies have shown that long noncoding RNA (IncRNA) gastric carcinoma highly expressed transcript 1 (GHET1) was involved in the progression of tumors. However, the role of GHET1 in esophageal squamous cell carcinoma (ESCC) remains unclear. Methods The expression of IncRNA GHET1 was examined in 55 paired ESCC tissues and adjacent nontumor tissues. Molecular and cellular techniques were used to explore the role of GHET1 on ESCC cells. Results Our data showed that GHET1 expression was significantly increased in ESCC tissues and cell lines. High GHET1 expression in ESCC tissues was significantly associated with poor differentiation, advanced tumor nodes metastasis stage, and lymph node metastasis. GHET1 showed high sensitivity and specificity for diagnosing ESCC. Our data from in vitro assays showed that GHET1 inhibition suppressed ESCC cells proliferation, migration, and invasion, and induced cells apoptosis. Furthermore, western blot showed that GHET1 inhibition significantly decreased the expression of vimentin and N-cadherin while it increased the expression of E-cadherin. Conclusions Our study indicates that GHET1 acts as an oncogene in ESCC and may represent a novel therapeutic target for the treatment of ESCC patients.


2018 ◽  
Vol 49 (6) ◽  
pp. 2511-2520 ◽  
Author(s):  
Zhonghua Zhang ◽  
Xuehai Wang ◽  
Shengda Cao ◽  
Xiao Han ◽  
Zhanwang Wang ◽  
...  

Background/Aims: Researchers have shown that long noncoding RNAs are closely associated with the pathogenesis of laryngeal squamous cell carcinoma (LSCC). However, the role of the long noncoding RNA taurine-upregulated gene 1 (TUG1) in the pathogenesis of LSCC remains unclear, although it is recognized as an oncogenic regulator for several types of squamous cell carcinoma. Methods: qRT-PCR was performed to measure the expression of TUG1 in LSCC tissues and cell lines. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) was used to measure the effect of TUG1 on cell proliferation. Transwell assay and flow cytometry were employed to determine the effect of TUG1 on cell migration and invasion. Western-blot were performed to explore the relation of TUG1 and p53 mRNA. Results: Higher TUG1 expression in LSCC than in paired normal tumor-adjacent tissue specimens (N = 64) was observed using quantitative real-time polymerase chain reaction. Also, high TUG1 expression was positively associated with advanced T category, worse lymph node metastasis and late clinical stage. Furthermore, in vitro experiments demonstrated that silencing of TUG1 markedly inhibited proliferation, cell-cycle progression, migration, and invasion of LSCC cells, whereas depletion of TUG1 led to increased apoptosis. Conclusion: These findings demonstrated that upregulated TUG1 expression exerted oncogenic effects by promoting proliferation, migration, and invasion, and inhibiting apoptosis in LSCC cells.


Oncotarget ◽  
2016 ◽  
Vol 7 (51) ◽  
pp. 84480-84485 ◽  
Author(s):  
Xuemei Chen ◽  
Hongyu Han ◽  
Yuqi Li ◽  
Qiongxia Zhang ◽  
Kailan Mo ◽  
...  

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