344 THE ROLE OF TRPV2 IN ESOPHAGEAL SQUAMOUS CELL CARCINOMA

2021 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Shunji Kato ◽  
Atsushi Shiozaki ◽  
Hitoshi Fujiwara ◽  
Hirotaka Konishi ◽  
Michihiro Kudou ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Basal Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Basal Cell ◽  
Immunohistochemical Staining ◽  
Migration And Invasion ◽  
Transient Receptor Potential Vanilloid

Abstract   Transient receptor potential vanilloid 2 (TRPV2) was recently shown to be involved in migrant potentials. Previous studies reported that TRPV2 was involved in cancer progression, migration, and invasion. The present study aimed to investigate its role in esophageal squamous cell carcinoma (ESCC). Methods In human ESCC cell lines, we investigated the role of TPRV2 in ESCC using a cancer function assay with the knockdown of TRPV2 by siRNA, microarray, pathway, and gene ontology analyses. The significance of TRPV2 expression in 62 ESCC samples was then evaluated by immunohistochemical staining. Results TRPV2 was overexpressed in TE15 and KYSE170 cells. TRPV2 depletion suppressed cell proliferation, cell cycle progression, and invasion/migration, and induced apoptosis. A pathway analysis of microarray data revealed that TRPV2 depletion down-regulated WNT/β-catenin signaling-related genes and basal cell carcinoma signaling-related genes. The suppression of cancer functions, such as proliferation, invasion, and angiogenesis, by TRPV2 depletion was predicted in the ontology analysis. Immunohistochemical staining revealed a relationship between strong TRPV2 expression and a poor prognosis in ESCC patients. Conclusion The present results suggest that TRPV2 regulates tumor progression by affecting WNT/β-catenin or basal cell carcinoma signaling, and that its strong expression is associated with a worse prognosis in ESCC patients. These results provide an insight into the role of TRPV2 as a therapeutic target or biomarker for ESCC.

scholarly journals The expression and role of TRPV2 in esophageal squamous cell carcinoma

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Michihiro Kudou ◽  
Atsushi Shiozaki ◽  
Yuzo Yamazato ◽  
Keita Katsurahara ◽  
Toshiyuki Kosuga ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Basal Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Basal Cell ◽  
Transient Receptor Potential ◽  
Expression Profiles ◽  
Transient Receptor Potential Vanilloid

Abstract Background: Transient receptor potential vanilloid 2 (TRPV2) was recently shown to be involved in migrant potentials. The present study aimed to investigate its role in esophageal squamous cell carcinoma (ESCC). Methods: Knockdown experiments were conducted using TRPV2 siRNA in human ESCC cell lines, and anti-tumor effects were analyzed. The gene expression profiles of cells were analyzed using a microarray method. An immunohistochemical staining was performed on 62 primary tumor samples. Results: TRPV2 overexpression was observed in TE15 and KYSE170 cells. TRPV2 depletion suppressed proliferation, cell cycle progression, and invasion/migration ability, and induced apoptosis. A pathway analysis of microarray data showed that TRPV2 depletion down-regulated WNT/β-catenin signaling-related genes and basal cell carcinoma signaling-related genes. The suppression of tumor functions, such as proliferation, invasion, and angiogenesis, was predicted in the ontology analysis. Immunohistochemical analysis revealed a correlation between strong TRPV2 expression and a poor prognosis in ESCC patients. Conclusion: The present results suggest that TRPV2 regulates cancer progression by affecting WNT/β-catenin or basal cell carcinoma signaling, and that TRPV2 strong expression is associated with a worse prognosis in ESCC patients. These results provide an insight into the role of TRPV2 as a novel therapeutic target or biomarker for ESCC.

PS02.201: EXPRESSION AND ROLE OF CLIC1 IN HUMAN ESOPHAGEAL SQUAMOUS CELL CARCINOMA

2018 ◽  
Vol 31 (Supplement_1) ◽  
pp. 179-179
Author(s):  
Toshiyuki Kobayashi ◽  
Atsushi Shiozaki ◽  
Hitoshi Fujiwara ◽  
Hirotaka Konishi ◽  
Yoshito Nako ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Microarray Analysis ◽  
Squamous Cell ◽  
Migration And Invasion ◽  
Poor Prognostic Factor ◽  
Weak Expression

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.

scholarly journals LncRNA GHET1 Promotes Esophageal Squamous Cell Carcinoma Cells Proliferation and Invasion via Induction of EMT

2017 ◽  
Vol 32 (4) ◽  
pp. 403-408 ◽  
Author(s):  
Hongfen Liu ◽  
Qiang Zhen ◽  
Yakun Fan
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Noncoding Rna ◽  
In Vitro Assays ◽  
Migration And Invasion ◽  
Advanced Tumor

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.

Geographic Pathology of Skin Cancer

1999 ◽  
Vol 3 (3) ◽  
pp. 120-122
Author(s):  
Robert Jackson
Keyword(s):  
Squamous Cell Carcinoma ◽  
Skin Cancer ◽  
Basal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Head And Neck ◽  
Squamous Cell ◽  
Basal Cell ◽  
Sun Exposure

Background: The development of knowledge concerning the role of sun exposure in causing skin cancer has been a gradual one. Objective: This article reviews the article by Urbach who used manikin coated with an ultraviolet dosimeter to see exactly where on the head and neck the exposure was greatest. Conclusion: Urbach showed that the areas of greatest sun exposure on his manikins corresponded with the location of 95% of squamous cell carcinoma and 66% of basal cell carcinoma. He also clearly showed the importance of scattered sky and reflected radiation.

Plasma miR-185 is decreased in patients with esophageal squamous cell carcinoma and might suppress tumor migration and invasion by targeting RAGE

2015 ◽  
Vol 309 (9) ◽  
pp. G719-G729 ◽  
Author(s):  
Rongrong Jing ◽  
Wen Chen ◽  
Huimin Wang ◽  
Shaoqing Ju ◽  
Hui Cong ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Biological Role ◽  
Migration And Invasion ◽  
High Level ◽  
Rage Expression

The receptor for advanced-glycation end products (RAGE) is upregulated in various cancers and has been associated with tumor progression, but little is known about its expression and regulation by microRNAs (miRNAs) in esophageal squamous cell carcinoma (ESCC). Here, we describe miR-185, which represses RAGE expression, and investigate the biological role of miR-185 in ESCC. In this study, we found that the high level of RAGE expression in 29 pairs of paraffin-embedded ESCC tissues was correlated positively with the depth of invasion by immunohistochemistry, suggesting that RAGE was involved in ESCC. We used bioinformatics searches and luciferase reporter assays to investigate the prediction that RAGE was regulated directly by miR-185. Besides, overexpression of miR-185 in ESCC cells was accompanied by 27% (TE-11) and 49% (Eca-109) reduced RAGE expression. The effect was further confirmed in RAGE protein by immunofluorescence in both cell lines. The effects were reversed following cotransfection with miR-185 and high-level expression of the RAGE vector. Furthermore, the biological role of miR-185 in ESCC cell lines was investigated using assays of cell viability, Ki-67 staining, and cell migration and invasion, as well as in a xenograft model. We found that overexpression of miR-185 inhibited migration and invasion by ESCC cells in vitro and reduced their capacity to develop distal pulmonary metastases in vivo partly through the RAGE/heat shock protein 27 pathway. Interestingly, in clinical specimens, the level of plasma miR-185 expression was decreased significantly ( P = 0.002) in patients with ESCC [0.500; 95% confidence interval (CI) 0.248–1.676] compared with healthy controls (2.410; 95% CI 0.612–5.671). The value of the area under the receiver-operating characteristic curve was 0.73 (95% CI 0.604–0.855). In conclusion, our findings shed novel light on the role of miR-185/RAGE in ESCC metastasis, and plasma miR-185 has potential as a novel diagnostic biomarker in ESCC.

miR-375 inhibits the proliferation, migration and invasion of esophageal squamous cell carcinoma by targeting XPR1

2020 ◽  
Vol 20 ◽  
Author(s):  
Wenbin Wu ◽  
Yangmei Zhang ◽  
Xiaowu Li ◽  
Xiang Wang ◽  
Yuan Yuan
Keyword(s):  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Promoting Effect ◽  
Dual Luciferase Assay ◽  
Invasion And Migration ◽  
And Migration

Objective: The purpose of this study was to explore the mechanism of the miR-375/XPR1 axis in esophageal squamous cell carcinoma (ESCC) and provide a new idea for targeted therapy of ESCC. Methods: Differentially expressed genes in GEO and TCGA databases were analyzed by bioinformatics. The expression levels of miR-375 and XPR1 mRNA were detected by qRT-PCR. Protein expression of XPR1 was detected by western blot. Bioinformatics analysis and dual luciferase assay were conducted to confirm the targeting relationship between miR-375 and XPR1. The viability, proliferation, migration and invasion of cells in each treatment group were detected by CCK-8, colony formation, wound healing and Transwell assays. Results: Significantly down-regulated miR-375 and remarkably up-regulated XPR1 were observed in ESCC tissue and cells. Overexpression of miR-375 inhibited proliferation, invasion and migration of ESCC cells, and greatly reduced the promoting effect of XPR1 overexpression on cell proliferation, migration and invasion. Dual luciferase assay confirmed that miR-375 targeted and inhibited XPR1 expression in ESCC. Conclusion: These results demonstrate the regulatory role of the miR-375/XPR1 axis in ESCC cells and provide a new potential target for the precise treatment of patients with ESCC.

Sign in / Sign up

Export Citation Format

Share Document