scholarly journals The ECM protein LTBP-2 is a suppressor of esophageal squamous cell carcinoma tumor formation but higher tumor expression associates with poor patient outcome

2010 ◽  
Vol 129 (3) ◽  
pp. 565-573 ◽  
Author(s):  
Stephen Ho Kin Chan ◽  
Josephine Mun Yee Ko ◽  
Kwok Wah Chan ◽  
Yuen Piu Chan ◽  
Qian Tao ◽  
...  
2018 ◽  
Vol 58 (1) ◽  
pp. 66-75 ◽  
Author(s):  
Chunyan Liu ◽  
Junyi Tang ◽  
Chang Li ◽  
Guangbo Pu ◽  
Dongxia Yang ◽  
...  

2021 ◽  
Author(s):  
Jacilene Martins Medeiros ◽  
Giuseppe Antônio Cirino ◽  
Arlindo Neto Montagnoli

2015 ◽  
Vol 117 (1) ◽  
pp. 118-125 ◽  
Author(s):  
Yuvaraj Sambandam ◽  
Sashank Sakamuri ◽  
Sundaravadivel Balasubramanian ◽  
Azizul Haque

2019 ◽  
Author(s):  
Fanghua Gong ◽  
Qiongzhen Chen ◽  
Jinmeng Li ◽  
Xiaoning Yang ◽  
Junfeng Ma ◽  
...  

Abstract Background: Loss of primary cilia is frequently observed in tumor cells, suggesting that the absence of this organelle may promote tumorigenesis through aberrant signal transduction, the inability to exit the cell cycle, and promotion of tumor cell invasion. Primary cilia loss also occurs in esophageal squamous cell carcinoma (ESCC) cells, but the molecular mechanisms that explain how ESCC cells lose primary cilia remain poorly understood. Methods: Inhibiting the expression of Prdx1 in the ESCC cells to detect the up-regulated genes related to cilium regeneration and down-regulated genes related to cilium disassembly by Gene chip. And, mice and cell experiments were carried to confirm the role of the HEF1-Aurora A-HDAC6 signaling axis in ESCC. Results: In this study, we found that silencing Peroxiredoxin 1 (Prdx1) restores primary cilia formation, and over-expressing Prdx1 induces primary cilia loss in ESCC cells. We also showed that the expression of Prdx1 regulates the action of the HEF1-Aurora A-HDAC6 signaling axis to promote the disassembly of primary cilia, and suppression of Prdx1 results in decreased tumor formation and tumor mass volume in vivo. Conclusions: These results suggest that Prdx1 is a novel regulator of primary cilia formation in ESCC cells.


2022 ◽  
Author(s):  
Bingbing Yang ◽  
Xiane Zhang ◽  
Hao Zhou ◽  
Xiaoyan Zhang ◽  
Wanjing Yang ◽  
...  

Abstract Background: Esophageal squamous cell carcinoma (ESCC) is a common malignant tumor of the digestive tract, which is very harmful to human health. The JAK-STAT signaling pathway is a recognized carcinogenic pathway that plays a role in the proliferation, apoptosis, migration, and invasion of a variety of cancer cells. Some studies have shown that the activation status of STAT3 affects the expression of KIRREL3. However, the expression of KIRREL3 in ESCC and its relationship with KIRREL3 or the JAK-STAT signaling pathway is still unclear.Methods: In this study, we used immunohistochemistry and western blotting to analyze the protein expression levels of KIRREL3 in tumor tissues and ESCC cell lines. We applied proliferation assays, plate clone formation assays, Transwell assays, flow cytometry analysis, and CDX animal models to examine the role of KIRREL3 in ESCC.Results: The results indicate that KIRREL3 is highly expressed to varying degrees in ESCC tissues and cell lines. Knocking down KIRREL3 expression in ESCC cells could correspondingly inhibit cell proliferation, colony formation, invasion, and migration, and had some effects on cell cycle progression and apoptosis. In addition, overexpressing KIRREL3 in these cells had opposite effects. Tumor formation in nude mice experiments also confirmed that KIRREL3 is involved in the growth of ESCC cells in vivo.Conclusions: These data suggest that KIRREL3 plays a key role in the development of ESCC, and KIRREL3 is a potential new target for the early diagnosis and clinical treatment of this disease.


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