Endocan: a new marker of endothelial function

Balta, Şevket; Balta, İlknur; Mikhailidis, Dimitri P.

doi:10.1097/hco.0000000000000867

Cited by 20 publications

(19 citation statements)

References 50 publications

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“…ESM1 is a 50 kDa soluble proteoglycan and is mainly secreted by vascular endothelial cells. In normal tissues, ESM1 is mainly expressed in vascular endothelial cells, distal renal tubular epithelial cells, and pulmonary endothelial cells, and is mainly involved in the in ammatory response [32] and angiogenesis [33]. Accumulative studies have shown that ESM1 was hyper-expressed in a variety of malignancies and was associated with tumor prognosis [34].…”

Section: Discussionmentioning

confidence: 99%

ESM1/VEGFα/ERK signaling axis augments cell proliferation and tumor angiogenesis in human cervical squamous cell carcinoma

Huang

et al. 2022

Preprint

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Background Aberrant expression of endothelial cell specific molecule 1 (ESM1) is frequent in the carcinogenesis of various neoplasms. However, the expression profile and prognostic value of ESM1 in CSCC remain ill-defined. Methods Human specimens were utilized to investigate the expression of ESM1 in normal cervical tissue, LSIL, HSIL, and CSCC samples by IHC and RT-qPCR assay. And, it was further validated and explored in CSCC based on GEO and TCGA datasets. Then, genomic enrichment analysis (GSEA) and in vitro experiments of human CSCC cell lines, including SiHa and ME-180, were applied to probe the potential molecular mechanisms of ESM1 in CSCC. Results In human samples, the ESM1 was hyper-expressed in CSCC, compared with the normal ones. Combined with TCGA and GEO, it further revealed that ESM1 was significantly overexpressed and related to dismal prognosis in CSCC patients. And, GSEA analysis showed that the tumor angiogenesis and the VEGFα signaling pathway were mostly enriched in CSCC patients with ESM1 high expression. Then, the in vitro experiment suggested that interference of ESM1 inhibited cell proliferation, migration, invasion, and enhanced apoptosis, resulting in the reduction of VEGFα expression and the phosphorylation of VEGFR2 (P-VEGFR2) and ERK-1/2 (P-ERK-1/2) in SiHa and ME-180 cells. Conclusions ESM1 is notably overexpressed in CSCC patients. Overexpression of ESM1 predicts an adverse prognosis of CSCC. Overexpressed ESM1 augments tumor angiogenesis and progression of CSCC via the VEGFα/ERK signaling pathway. Thus, ESM1 and related genes may serve as promising prognostic biomarkers or candidate therapeutic targets for CSCC patients.

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Section: Discussionmentioning

confidence: 99%

ESM1/VEGFα/ERK signaling axis augments cell proliferation and tumor angiogenesis in human cervical squamous cell carcinoma

Huang

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…ESM1 is a 50 kDa soluble proteoglycan and is mainly secreted by vascular endothelial cells. In normal tissues, ESM1 is mainly expressed in vascular endothelial cells, distal renal tubular epithelial cells and pulmonary endothelial cells, and is mainly involved in the in ammatory response [33] and angiogenesis [34]. Accumulative studies have shown that ESM1 was hyper-expressed in a variety of malignancies and is associated with tumor prognosis [35].…”

Section: Discussionmentioning

confidence: 99%

ESM1/VEGFα signaling pathway augments endothelial cell proliferation and tumor angiogenesis in human cervical squamous cell carcinoma

Huang

et al. 2022

Preprint

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Background The aberrant expression of endothelial cell specific molecule 1 (ESM1) is frequent in the carcinogenesis of various neoplasms. However, the expression profile, potential biological function and prognostic value of ESM1 in CSCC remain undetermined. Methods In the present study, we used human specimens to investigate the expression pattern of ESM1 in normal cervical tissue, LSIL, HSIL and CSCC samples by IHC assay and RT-qPCR. The expression pattern and the diagnostic or prognostic value of ESM1 were then further validated and explored in CSCC based on GEO and TCGA. Genomic enrichment analysis (GSEA) was applied to probe the masked molecular mechanisms of ESM1 in CSCC. Finally, the molecular mechanisms of ESM1 in human CSCC cell lines, including SiHa and ME-180 cells, were explored by in vitro studies of RNA interference experiments. Results In human samples, the ESM1 was significantly hyper-expressed in CSCC or HSIL, compared with LSIL or normal cervical tissue. The data from TCGA and GEO further confirmed that ESM1 was overexpressed in CSCC and was significantly related to dismal overall survival (OS) in CSCC patients. Furthermore, GSEA analysis showed that the CSCC patients with ESM1high were mostly enriched in angiogenesis and the VEGFα signaling pathway. Finally, the in vitro experiment suggested that interference of ESM1 inhibited the cell proliferation, migration, invasion and enhanced apoptosis, resulting in the reduction of VEGFα expression, HIF-1α expression, the phosphorylation of VEGFR2 (P-VEGFR2) and ERK-1/2 (P-ERK-1/2) in SiHa and ME-180 cells. Conclusion This assay figures out that ESM1 is notably overexpressed in CSCC patients. Overexpression of ESM1 predicts adverse prognosis of CSCC, and overexpressed ESM1, VEGFα and HIF-1α harbored synergistic effect in tumorigenesis and progression of CSCC cells through the VEGFα/VEGFR2/ERK signaling pathway. Thus, ESM1 and related genes may serve as promising diagnostic or prognostic biomarkers and candidate therapeutic targets for CSCC patients.

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“…Endothelial Cell-Specific Molecule 1 (Endocan) is a new immunoinflammatory marker that may be associated with cardiovascular events. 68 Some cardiovascular diseases and related conditions, are associated with raised endocan levels. 69 Furthermore, it is possible that endothelial injury, activation, and dysfunction are caused by oxidative stress in the relationship between the HT and endothelial dysfunction.…”

Section: Atherosclerosis Markers and Non-alcoholic Fatty Liver Diseasementioning

confidence: 99%

Atherosclerosis and Non-Alcoholic Fatty Liver Disease

Balta

2022

Angiology

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Non-alcoholic fatty liver disease (NAFLD) is a common disease defined by excess fat deposition in the liver. The course of NAFLD is not fully understood, however, some pathogenic mechanisms have been identified. Accumulation of fat in liver cells is associated with insulin resistance, central obesity, triglyceride accumulation in the liver and hepatic fatty acid metabolism dysregulation that cause steatosis. The other process leads to hepatocyte inflammation and necrosis, which leads to severe hepatic disease; non-alcoholic steatohepatitis. Many clinical studies have underlined the link between NAFLD and atherosclerosis. NAFLD may alter the balance lipid-glucose metabolism as well as increase the risk of hypertension and systemic inflammation. This results in a greater risk of vascular events. The present review considers the link between NAFLD and atherosclerosis.

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Endocan: a new marker of endothelial function

Cited by 20 publications

References 50 publications

ESM1/VEGFα/ERK signaling axis augments cell proliferation and tumor angiogenesis in human cervical squamous cell carcinoma

ESM1/VEGFα/ERK signaling axis augments cell proliferation and tumor angiogenesis in human cervical squamous cell carcinoma

ESM1/VEGFα signaling pathway augments endothelial cell proliferation and tumor angiogenesis in human cervical squamous cell carcinoma

Atherosclerosis and Non-Alcoholic Fatty Liver Disease

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