Snail promotes the generation of vascular endothelium by breast cancer cells

Chang, Zhenyu; Zhang, Yanan; Liu, Jie; Zheng, Yu; Li, Huayue; Kong, Yan; Li, Pengyun; Peng, Haiwen; Shi, Yajiao; Cao, Bo; Ran, Fang; Chen, Yingjie; Song, Yuhua; Ye, Qinong; Ding, Lihua

doi:10.1038/s41419-020-2651-5

Cited by 10 publications

(6 citation statements)

References 34 publications

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“…The sequences of the miR-377-3p probe and U6 positive control were shown in Table S1. Immunohistochemistry (IHC) of formalin-fixed paraffin-embedded samples was performed as described previously [ 30 ]. Mouse anti-CPT1C was used at dilutions of 1:200 for IHC.…”

Section: Methodsmentioning

confidence: 99%

MicroRNA-377-3p inhibits hepatocellular carcinoma growth and metastasis through negative regulation of CPT1C-mediated fatty acid oxidation

Zhang

Liu

et al. 2022

Cancer Metab

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Background Altered lipid metabolism is closely related to the occurrence and development of hepatocellular carcinoma (HCC). Carnitine palmitoyltransferase 1C (CPT1C) is a member of CPT1 family and plays a key role in cancer development and progression. However, how microRNAs (miRNAs) regulate CPT1C-mediated fatty acid transport and oxidation remains to be elucidated. Methods Oil Red O staining, mitochondrial, and lipid droplets immunofluorescence staining were used to detect the functions of miR-377-3p and CPT1C in fatty acid oxidation. Colocalization of palmitate and mitochondria was performed to investigate the function of miR-377-3p and CPT1C in fatty acid transport into mitochondria. Fatty acid oxidation (FAO) assay was used to detect the function of miR-377-3p and CPT1C in FAO. Cell proliferation, migration and invasion assays and animal experiments were used to evaluate the role of miR-377-3p/CPT1C axis in HCC progression in vitro and in vivo. Immunofluorescence staining was used to identify the clinical significance of miR-377-3p and CPT1C in HCC patients. Results MiR-377-3p inhibits CPT1C expression by targeting its 3’-untranslated region. Through repression of CPT1C, miR-377-3p suppresses fatty acid oxidation by preventing fatty acid from entering into mitochondria and decreasing ATP production in HCC cells. Inhibiting fatty acid oxidation abolishes the ability of miR-377-3p/CPT1C axis to regulate HCC proliferation, migration, invasion and metastasis in vitro and in vivo. In HCC patients, CPT1C is significantly upregulated, and miR-377-3p expression and lipid droplets are negatively correlated with CPT1C expression. High expression of miR-377-3p and CPT1C predict better and worse clinical outcomes, respectively. Conclusions We uncover the key function and the relevant mechanisms of the miR-377-3p/CPT1C axis in HCC, which might provide a potential target for the treatment of HCC.

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Section: Methodsmentioning

confidence: 99%

MicroRNA-377-3p inhibits hepatocellular carcinoma growth and metastasis through negative regulation of CPT1C-mediated fatty acid oxidation

Zhang

Liu

et al. 2022

Cancer Metab

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“…Because acetylation masks the positive charge on lysine residues and weakens the DNA-histone association and relaxes the chromatin structure, histone acetylation is often associated with gene activation. SNAI1 recruits the p300 activator complex to the VEGF and Sox2 promoters to stimulate their expression, leading to endothelium generation and tumor growth [70].…”

Section: Acetylationmentioning

confidence: 99%

Epigenetic Regulation and Post-Translational Modifications of SNAI1 in Cancer Metastasis

Dong

2021

IJMS

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SNAI1, a zinc finger transcription factor, not only acts as the master regulator of epithelial-mesenchymal transition (EMT) but also functions as a driver of cancer progression, including cell invasion, survival, immune regulation, stem cell properties, and metabolic regulation. The regulation of SNAI1 occurs at the transcriptional, translational, and predominant post-translational levels including phosphorylation, acetylation, and ubiquitination. Here, we discuss the regulation and role of SNAI1 in cancer metastasis, with a particular emphasis on epigenetic regulation and post-translational modifications. Understanding how signaling networks integrate with SNAI1 in cancer progression will shed new light on the mechanism of tumor metastasis and help develop novel therapeutic strategies against cancer metastasis.

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“…Nevertheless, little is known about the interaction between NETs and platelet activation in GC patients. Venous endothelial cell (EC) injury in cancer patients is also closely related to venous thrombosis[ 26 , 27 ]. Interestingly, the cytotoxicity of NETs against ECs enhances PCA in oral squamous cancer, even in patients with obstructive jaundice and inflammatory bowel disease[ 28 - 30 ].…”

Section: Introductionmentioning

confidence: 99%

Neutrophil extracellular traps participate in the development of cancer-associated thrombosis in patients with gastric cancer

Li¹,

Zou²,

Yang³

et al. 2022

WJG

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BACKGROUND The development of venous thromboembolism (VTE) is associated with high mortality among gastric cancer (GC) patients. Neutrophil extracellular traps (NETs) have been reported to correlate with the prothrombotic state in some diseases, but are rarely reported in GC patients. AIM To investigate the effect of NETs on the development of cancer-associated thrombosis in GC patients. METHODS The levels of NETs in blood and tissue samples of patients were analyzed by ELISA, flow cytometry, and immunofluorescence staining. NET generation and hypercoagulation of platelets and endothelial cells (ECs) in vitro were observed by immunofluorescence staining. NET procoagulant activity (PCA) was determined by fibrin formation and thrombin–antithrombin complex (TAT) assays. Thrombosis in vivo was measured in a murine model induced by flow stenosis in the inferior vena cava (IVC). RESULTS NETs were likely to form in blood and tissue samples of GC patients compared with healthy individuals. In vitro studies showed that GC cells and their conditioned medium, but not gastric mucosal epithelial cells, stimulated NET release from neutrophils. In addition, NETs induced a hypercoagulable state of platelets by upregulating the expression of phosphatidylserine and P-selectin on the cells. Furthermore, NETs stimulated the adhesion of normal platelets on glass surfaces. Similarly, NETs triggered the conversion of ECs to hypercoagulable phenotypes by downregulating the expression of their intercellular tight junctions but upregulating that of tissue factor. Treatment of normal platelets or ECs with NETs augmented the level of plasma fibrin formation and the TAT complex. In the models of IVC stenosis, tumor-bearing mice showed a stronger ability to form thrombi, and NETs abundantly accumulated in the thrombi of tumor-bearing mice compared with control mice. Notably, the combination of deoxyribonuclease I, activated protein C, and sivelestat markedly abolished the PCA of NETs. CONCLUSION GC-induced NETs strongly increased the risk of VTE development both in vitro and in vivo . NETs are potential therapeutic targets in the prevention and treatment of VTE in GC patients.

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Snail promotes the generation of vascular endothelium by breast cancer cells

Cited by 10 publications

References 34 publications

MicroRNA-377-3p inhibits hepatocellular carcinoma growth and metastasis through negative regulation of CPT1C-mediated fatty acid oxidation

MicroRNA-377-3p inhibits hepatocellular carcinoma growth and metastasis through negative regulation of CPT1C-mediated fatty acid oxidation

Epigenetic Regulation and Post-Translational Modifications of SNAI1 in Cancer Metastasis

Neutrophil extracellular traps participate in the development of cancer-associated thrombosis in patients with gastric cancer

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