scholarly journals Pancreatic Cancer-Induced Neutrophil Extracellular Traps: A Potential Contributor to Cancer-Associated Thrombosis

2017 ◽  
Vol 18 (3) ◽  
pp. 487 ◽  
Author(s):  
Norbaini Abdol Razak ◽  
Omar Elaskalani ◽  
Pat Metharom
Keyword(s):  
Pancreatic Cancer ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Traps ◽  
Potential Contributor ◽  
Cancer Associated Thrombosis

scholarly journals The Emerging Role of Neutrophil Extracellular Traps in Arterial, Venous and Cancer-Associated Thrombosis

2021 ◽  
Vol 8 ◽  
Author(s):  
Yilu Zhou ◽  
Weimin Tao ◽  
Fuyi Shen ◽  
Weijia Du ◽  
Zhendong Xu ◽  
...  
Keyword(s):  
Current Knowledge ◽  
Neutrophil Extracellular Traps ◽  
Vital Role ◽  
Extracellular Traps ◽  
Protein Components ◽  
Cancer Associated Thrombosis ◽  
Coagulation Pathway

Neutrophils play a vital role in the formation of arterial, venous and cancer-related thrombosis. Recent studies have shown that in a process known as NETosis, neutrophils release proteins and enzymes complexed to DNA fibers, collectively called neutrophil extracellular traps (NETs). Although NETs were originally described as a way for the host to capture and kill bacteria, current knowledge indicates that NETs also play an important role in thrombosis. According to recent studies, the destruction of vascular microenvironmental homeostasis and excessive NET formation lead to pathological thrombosis. In vitro experiments have found that NETs provide skeletal support for platelets, red blood cells and procoagulant molecules to promote thrombosis. The protein components contained in NETs activate the endogenous coagulation pathway to promote thrombosis. Therefore, NETs play an important role in the formation of arterial thrombosis, venous thrombosis and cancer-related thrombosis. This review will systematically summarize and explain the study of NETs in thrombosis in animal models and in vivo experiments to provide new targets for thrombosis prevention and treatment.

scholarly journals AB080. P052. Role of neutrophil extracellular traps (NETs) in pancreatic cancer liver metastasis

2018 ◽  
Vol 1 (1) ◽  
pp. AB080-AB080
Author(s):  
Shin Takesue ◽  
Kenoki Ohuchida ◽  
Hiromichi Nakayama ◽  
Kazuhiro Koikawa ◽  
Koji Shindo ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Liver Metastasis ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Traps

scholarly journals Targeting neutrophil extracellular traps with thrombomodulin prevents pancreatic cancer metastasis

2021 ◽  
Vol 497 ◽  
pp. 1-13
Author(s):  
Hiroki Kajioka ◽  
Shunsuke Kagawa ◽  
Atene Ito ◽  
Masashi Yoshimoto ◽  
Shuichi Sakamoto ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Metastasis ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Traps

Sciellin stimulates gallbladder cancer proliferation and tumor-association thrombosis via formation of neutrophil extracellular traps

2020 ◽  
Author(s):  
Yang Li ◽  
Tai Ren ◽  
Bo Yang ◽  
Huijie Miao ◽  
Liguo Liu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Gallbladder Cancer ◽  
Cell Biology ◽  
Tumor Development ◽  
Neutrophil Extracellular Traps ◽  
Cancer Proliferation ◽  
Extracellular Traps ◽  
Egfr Expression ◽  
Tumor Association ◽  
Cancer Associated Thrombosis

Abstract Background：Apart from primary tumor development and metastasis, cancer-associated thrombosis is the second cause of cancer death in solid tumor malignancy. However, the mechanistic insight into the development of gallblader cancer (GBC) and cancer-associated thrombosis remains unclear. This study aimed to investigate the mechanistic role of Sciellin （SCEL） in GBC cell proliferation and the development of venous thromboembolism. Methods: The expression level of SCEL was determined by immunohistochemical staining. Roles of SCEL in gallbladder cancer cell were determined by molecular and cell biology methodsResults: SCEL was markedly upregulated in GBC and associated with advanced TNM stages and a poor prognosis. Furthermore, SCEL interacted with EGFR and stabilized EGFR expression that activates downstream PI3K and Akt pathway, leading to cell proliferation. In addition, SCEL induces tumor cell IL-8 production that stimulates the formation of neutrophil extracellular traps (NETs), accelerating thromboembolism. In xenografts, SCEL-expressing GBCs developed larger tumors and thrombosis compared with control cells. Conclusions: The present results indicate that SCEL promotes GBC cell proliferation and induces NET-associated thrombosis , thus serving as a potential therapeutic target.

scholarly journals Tumor-Derived Exosomes Induce the Formation of Neutrophil Extracellular Traps: Implications For The Establishment of Cancer-Associated Thrombosis

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Ana C. Leal ◽  
Daniella M. Mizurini ◽  
Tainá Gomes ◽  
Natalia C. Rochael ◽  
Elvira M. Saraiva ◽  
...  
Keyword(s):  
Neutrophil Extracellular Traps ◽  
Extracellular Traps ◽  
Cancer Associated Thrombosis

scholarly journals Role of Sciellin in gallbladder cancer proliferation and formation of neutrophil extracellular traps

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Yang Li ◽  
Ruiyan Yuan ◽  
Tai Ren ◽  
Bo Yang ◽  
Huijie Miao ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Gallbladder Cancer ◽  
Cell Biology ◽  
Tumor Development ◽  
Neutrophil Extracellular Traps ◽  
Cancer Proliferation ◽  
Extracellular Traps ◽  
Egfr Expression ◽  
Cancer Associated Thrombosis

AbstractApart from primary tumor development and metastasis, cancer-associated thrombosis is the second cause of cancer death in solid tumor malignancy. However, the mechanistic insight into the development of gallbladder cancer (GBC) and cancer-associated thrombosis remains unclear. This study aimed to investigate the mechanistic role of Sciellin (SCEL) in GBC cell proliferation and the development of venous thromboembolism. The expression level of SCEL was determined by immunohistochemical staining. Roles of SCEL in gallbladder cancer cell were determined by molecular and cell biology methods. SCEL was markedly upregulated in GBC and associated with advanced TNM stages and a poor prognosis. Furthermore, SCEL interacted with EGFR and stabilized EGFR expression that activates downstream PI3K and Akt pathway, leading to cell proliferation. In addition, SCEL induces tumor cell IL-8 production that stimulates the formation of neutrophil extracellular traps (NETs), accelerating thromboembolism. In xenografts, SCEL-expressing GBCs developed larger tumors and thrombosis compared with control cells. The present results indicate that SCEL promotes GBC cell proliferation and induces NET-associated thrombosis, thus serving as a potential therapeutic target.

scholarly journals Ddr1-induced neutrophil extracellular traps drive pancreatic cancer metastasis

JCI Insight ◽  
2021 ◽  
Author(s):  
Jenying Deng ◽  
Ya'an Kang ◽  
Chien-Chia Cheng ◽  
Xinqun Li ◽  
Bingbing Dai ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cancer Metastasis ◽  
Neutrophil Extracellular Traps ◽  
Extracellular Traps

scholarly journals The regulatory mechanism of neutrophil extracellular traps in cancer biological behavior

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hui Wang ◽  
Yiyin Zhang ◽  
Qianling Wang ◽  
Xiaoli Wei ◽  
Hua Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Host Defense ◽  
Regulatory Mechanism ◽  
Neutrophil Extracellular Traps ◽  
Biological Behavior ◽  
Molecular Pathways ◽  
The Past ◽  
Extracellular Traps ◽  
Promote Tumor Growth ◽  
Cancer Associated Thrombosis

AbstractAs the predominant host defense against pathogens, neutrophil extracellular traps (NETs) have attracted increasing attention due to their vital roles in infectious inflammation in the past few years. Interestingly, NETs also play important roles in noninfectious conditions, such as rheumatism and cancer. The process of NETs formation can be regulated and the form of cell death accompanied by the formation of NETs is regarded as “NETosis”. A large amount of evidence has confirmed that many stimuli can facilitate the release of NETs from neutrophils. Furthermore, it has been illustrated that NETs promote tumor growth and progression via many molecular pathways. Meanwhile, NETs also can promote metastasis in many kinds of cancers based on multiple studies. In addition, some researchs have found that NETs can promote coagulation and cancer-associated thrombosis. In the present review, it will highlight how NETosis, which is stimulated by various stimuli and signaling pathways, affects cancer biological behaviors via NETs. Given their crucial roles in cancer, NETs will become possible therapeutic targets for inhibiting proliferation, metastasis and thrombosis in cancer patients.

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