Endocan reduces the malign grade of gastric cancer cells by regulating associated protein expression

Chen, Shaolong; Wei, Xiang; Qi, Yinliang; Zhou, Qing; Wang, Yuan

doi:10.1007/s13277-016-5398-y

Cited by 10 publications

(10 citation statements)

References 24 publications

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“…When Fas binds to the Fas-L, it recruits several adapter proteins and forms the death-inducing signaling complex, eventually activating caspase-3, 6, 7 and inducing apoptosis. 20 , 34 , 35 Previous studies have shown that endocan can be involved in cell apoptosis through mitochondrial unfolded protein response and caspase- and p53-dependent apoptotic pathway. 19 , 20 Abnormal structural cell apoptosis in COPD leads to destruction of terminal airways, alveolar walls and pulmonary capillary beds, and is an important mechanism involved in the development of COPD.…”

Section: Discussionmentioning

confidence: 99%

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The association of elevated circulating endocan levels with lung function decline in COPD patients

Dai

Chen

et al. 2018

COPD

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BackgroundEndocan is thought to be a novel inflammatory marker that is associated with a variety of inflammatory diseases. However, its role in the pathogenesis of COPD remains unclear. This study aims to explore the potential role of endocan in COPD.MethodsIn total, 27 healthy volunteers, 55 COPD patients and 36 acute exacerbation of chronic obstructive pulmonary disease (AECOPD) patients were included in the study. Basic demographic characteristics, clinical features and blood samples were collected. Magnetic luminex screening assays were used to detect the concentration of endocan, Fas and Fas ligand (Fas-L) in plasma. Differences between groups were compared using an Independent sample t-test, Welch’s t-test, chi-squared test and Wilcoxon rank sum test. The correlations of plasma endocan with lung function parameters, Fas and Fas-L were analyzed by Pearson’s partial correlation test (adjusted for age, gender, body mass index and smoking history) and multiple linear regression.ResultsPlasma endocan levels in COPD patients were significantly higher than those in healthy volunteers (509.7±18.25 pg/mL vs 434.8±18.98 pg/mL (P=0.0124)), and AECOPD patients had the highest levels of endocan (524.7±27.18 pg/mL). Correlation analysis showed that circulating endocan had a negative correlation to FEV1/FVC, FEV1/predictive and FVC (adjusted r=−0.213, P=0.03; adjusted r=−0.209, P=0.034; and adjusted r=−0.300, P=0.002, respectively), and had a positive correlation to Fas (adjusted r=0.280, P=0.004).ConclusionOur study shows that elevated circulating endocan levels are associated with reduced lung ventilation function in COPD and AECOPD patients. In addition, endocan may influence apoptosis in COPD, suggesting that endocan may play a role in COPD pathogenesis.

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Section: Discussionmentioning

confidence: 99%

“… 17 , 18 Endocan can relieve the apoptosis of lung epithelial cell in acute lung injury (ALI) by releasing over-activated mitochondrial unfolded protein response; endocan also promotes the differentiation and apoptosis of gastric adenocarcinoma cell by activating caspase- and p53-dependent apoptotic pathway. 19 , 20 …”

Section: Introductionmentioning

confidence: 99%

The association of elevated circulating endocan levels with lung function decline in COPD patients

Dai

Chen

et al. 2018

COPD

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“…Recently, endocan has been identified to be overexpressed at the messenger RNA and/or protein levels in several tumor types, including glioblastoma, nonsmall cell lung cancer, gastric cancer, and hepatocellular carcinoma [13,47,48]. Most evidence suggested that endocan overexpression contributed to aggressive tumor progression and poor outcomes [9,49,50].…”

Section: Discussionmentioning

confidence: 99%

“…Endocan was originally described as being secreted by human umbilical vein endothelial cells (HUVECs) [8]. Recently, endocan has been identified to be upregulated in various tumors [9][10][11]. In addition, endocan has also been found in common brain tumors and acted as a marker for malignancy [12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Prediction and identification of novel HLA-A*0201-restricted cytotoxic T lymphocyte epitopes from endocan

Shao¹,

Liu²,

Yang³

et al. 2020

J Inflamm

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Background: Prediction and identification of cytotoxic T lymphocyte (CTL) epitopes from tumor associated antigens is a crucial step for the development of tumor immunotherapy strategy. Endocan has been identified as antigen overexpressed in various tumors. Methods: In this experiment, we predicted and identified HLA-A2-restricted CTL epitopes from endocan by using the following procedures. Firstly, we predicted the epitopes from the amino acid sequence of endocan by computer-based methods; Secondly, we determined the affinity of the predicted peptide with HLA-A2.1 molecule by peptide-binding assay; Thirdly, we elicited the primary T cell response against the predicted peptides in vitro; Lastly, we tested the specific CTLs toward endocan and HLA-A2.1 positive target cells. Results: These data demonstrated that peptides of endocan containing residues 4-12 and 9-17 could elicit specific CTLs producing interferon-γ and cytotoxicity. Conclusions: Therefore, our findings suggested that the predicted peptides were novel HLA-A2.1-restricted CTL epitopes, and might provide promising target for tumor immunotherapy.

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“…Therefore, ENDOCAN may be involved in the autophagy of leukemia cells. Other tumor growth-related pathways, including p53, epidermal growth factor receptor (EGFR), vascular EGFR type 2, phosphoinositide 3-kinase, Akt and mammalian target of rapamycin are also regulated by ENDOCAN (42,43). These pathways may also be involved in ENDOCAN-mediated proliferation and apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of ENDOCAN in myeloid leukemia cells inhibits proliferation and promotes apoptosis by suppressing nuclear factor‑κB activity

Sun

et al. 2019

Mol Med Report

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Previous studies have demonstrated that ENDOCAN is elevated in leukemia, and it has been reported to be associated with poor prognosis. However, the functional role of ENDOCAN in the development of leukemia remains to be fully elucidated. In the present study, the expression levels of ENDOCAN were detected in THP-1, U937, HL-60 and K562 cells, and it was found that ENDOCAN was increased in U937 and K562 cells, compared with the other two cell lines. Subsequently, ENDOCAN was knocked down in U937 and K562 cells via lentiviral infection. It was found that cell proliferation and the expression of proliferating cell nuclear antigen were inhibited in myeloid leukemia cells following the silencing of ENDOCAN. ENDOCAN knockdown induced G0/G1-phase cell cycle arrest in myeloid leukemia cells with a decreased expression of cyclin D1. Furthermore, cell apoptosis was increased in response to ENDOCAN silencing, which was accompanied by the downregulation of B-cell lymphoma (BCL2) and the upregulation of BCL2-associated X protein, cleaved caspases 3 and 9, and cleaved poly (ADP-ribose) polymerase. Furthermore, it was demonstrated that the knockdown of ENDOCAN inhibited nuclear factor-κB (NF-κB) activity, as evidenced by the increased expression of NF-κB inhibitor α (IκBα), decreased expression of phosphorylated (p-)IκBα, p-P65 and nuclear P65, and reduced NF-κB DNA-binding activity. In combination, the present findings suggested that ENDOCAN may serve as a potential therapeutic target in the treatment of leukemia.

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Endocan reduces the malign grade of gastric cancer cells by regulating associated protein expression

Cited by 10 publications

References 24 publications

The association of elevated circulating endocan levels with lung function decline in COPD patients

The association of elevated circulating endocan levels with lung function decline in COPD patients

Prediction and identification of novel HLA-A*0201-restricted cytotoxic T lymphocyte epitopes from endocan

Downregulation of ENDOCAN in myeloid leukemia cells inhibits proliferation and promotes apoptosis by suppressing nuclear factor‑κB activity

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