Endocan is a stable circulating molecule in ICU patients

Publication date: Available online 18 April 2017
Source:Clinical Biochemistry
Author(s): Gaudet Alexandre, Chenevier-Gobeaux Camille, Parmentier Erika, Delobel Jean-Edouard, Dubucquoi Sylvain, Mathieu Daniel, Lassalle Philippe, De Freitas Caires Nathalie
BackgroundEndocan is a lung endothelial cell secreted proteoglycan, possessing multiple physiological roles and potential therapeutic and diagnostic utility as biomarker in pneumonia and acute respiratory distress syndrome. Endocan synthesis and secretion can be induced by proinflammatory cytokines such as TNF-α, but can also be subject of proteolytic degradation causing preanalytical variation.MethodsWe investigated the stability of endocan in conventional serum, plasma, anticoagulated whole blood, as well as whole blood and plasma stabilized with protease inhibitors.ResultsAmong the recipient tubes for blood collection, those with EDTA gave minimal interference. No dilution effect was observed on recovery tests from 1:2 to 1:16 (v:v). The recovery test in 10 plasma EDTA samples from healthy subjects or septic patients indicated a median recovery of 104.5% [104%–107.5%], and 97% [88.5%; 102.5%], respectively. Patient's plasma endocan remains stable when stored at room temperature till 72h, or following 3 freeze thaw cycles. Finally, no interference was observed with hemolytic, icteric or turbidic plasma samples.ConclusionThese results are consistent with the view that endocan measured in ICU patients is intact, stable, and accurate. Then, the low endocan level observed in ICU patients who developed ARDS is likely to be reliable.



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Celiac disease

Celiac disease: A disorder resulting from an immune reaction to gluten, a protein found in wheat and related grains, and present in many foods. Celiac disease causes impaired absorption and digestion of nutrients through the small intestine. Symptoms include frequent diarrhea , weight loss , iron deficiency anemia, osteoporosis . A skin condition dermatitis herpetiformis can be associated with celiac disease. The most accurate test for celiac disease is a biopsy of the small bowel usually performed by an endoscopy (tube passed into the intestine through the mouth). Treatment is to avoid gluten in the diet. Medications may be used for refractory (stubborn) celiac disease.

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Asporin promotes pancreatic cancer cell invasion and migration by regulating the epithelial-to-mesenchymal transition (EMT) through both autocrine and paracrine mechanisms

Publication date: 10 July 2017
Source:Cancer Letters, Volume 398
Author(s): Lili Wang, Huanwen Wu, Li Wang, Hui Zhang, Junliang Lu, Zhiyong Liang, Tonghua Liu
Pancreatic cancer is histopathologically characterized by excessive desmoplasia induced by pancreatic stellate cells (PSCs). Asporin, an extracellular matrix (ECM) protein, is highly expressed in cancer-associated fibroblasts (CAFs). Asporin expression in PSCs and its roles in PSC-pancreatic cancer cell (PCC) interaction remain unclear. The present study firstly showed that Asporin is highly expressed in activated PSCs and is involved in PSC-mediated invasion and migration of PCCs. Exogenous Asporin interacted with the transmembrane receptor CD44 on PCCs to activate NF-κB/p65 and promoted the epithelial–mesenchymal transition (EMT) in PCCs. Furthermore, AKT and ERK pathways participated in Asporin/CD44-induced NF-κB/p65 activation in pancreatic cancer. Asporin had similar effects on PCCs via an autocrine mechanism. Consistent with our in vitro experiments, we showed that Asporin in peritumoral stroma of pancreatic cancer tissues was associated with poor clinical outcome. In conclusion, this is the first study to show that Asporin promotes EMT, invasion, and migration of PCCs by activating CD44-AKT/ERK-NF-κB pathway in paracrine and autocrine manners. Moreover, our results indicate that Asporin may be a prognostic marker and suggest that targeting the tumor microenvironment represents a promising therapeutic strategy in pancreatic cancer.



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ZEB1 induced miR-99b/let-7e/miR-125a cluster promotes invasion and metastasis in esophageal squamous cell carcinoma

Publication date: 10 July 2017
Source:Cancer Letters, Volume 398
Author(s): Jianlin Ma, Yun Zhan, Zhipeng Xu, Yi Li, Aiping Luo, Fang Ding, Xiufeng Cao, Hongyan Chen, Zhihua Liu
Esophageal squamous cell carcinoma (ESCC) is one of the most common digestive tumors in Asia. Recent researches demonstrate that miRNAs are involved in the development of ESCC. In this study, we identified a miRNA cluster, termed miR-99b/let-7e/miR-125a as pro-metastasis oncomir. Overexpression of this miRNA cluster promoted ESCC cell migration and invasion in vitro and induced an experimental metastasis in vivo. ZEB1 was discovered to bind to the promoter region of miR-99b/let-7e/miR-125a cluster and regulate the expression of miRNAs at transcriptional level. Knockdown of ZEB1 resulted in a decrease of both mature and primary miRNAs. Further research revealed AT-rich interaction domain 3A (ARID3A) as a direct target of miR-99b/let-7e/miR-125a cluster. Reduced ARID3A phenocopied miR-99b/let-7e/miR-125a overexpression, and elevated ARID3A counteracted the pro-metastasis effect of miR-99b/let-7e/miR-125a. Moreover, ARID3A was downregulated by ZEB1 in a miR-99b/let-7e/miR-125a dependent manner. Collectively, our study sheds light on the essential role of miR-99b/let-7e/miR-125a cluster in tumor metastasis.



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Down-regulation of DLC1 in endothelial cells compromises the angiogenesis process

Publication date: 10 July 2017
Source:Cancer Letters, Volume 398
Author(s): Yi-Ping Shih, Sarah Y. Yuan, Su Hao Lo
DLC1 is a RhoGAP-containing tumor suppressor that inhibits angiogenesis by repressing VEGF production in epithelial cells. Here we report the roles of DLC1 in endothelial cells. Silencing of DLC1 (siDLC1) enhances cell migration but reduces tube formation activities of human umbilical vein endothelial cells (HUVECs). Biochemically, RhoA activity and paxillin protein level are markedly increased in siDLC1 HUVECs. Although further silencing of RhoA restores the cell migration phenotype, the tube formation defect and up-regulated paxillin level remain unchanged. On the other hand, paxillin knockdown rescues tube formation and migration phenotypes but not the up-regulated RhoA activity. These results indicate that DLC1 regulates endothelial cell migration through RhoA and paxillin independently and controls tube formation mainly via paxillin. To further determine endothelial DLC1's function, we have generated endothelial specific knockout mice (DLC1-Tek). DLC1-Tek mice appear to be normal and healthy but their angiogenesis processes are compromised as shown in gel plug and aortic ring sprouting assays. Analysis of endothelial cells isolated from DLC1-Tek mice has further affirmed the cellular and biochemical phenotypes established in siDLC1 HUVECs. Our studies have demonstrated a positive regulatory role of endothelial DLC1 in angiogenesis.



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Fighting pancreatic cancer

Publication date: 10 July 2017
Source:Cancer Letters, Volume 398
Author(s): Min Li




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New blood test offers potential for faster, targeted treatment of NSCLC

Identification of a specific genetic mutation in patients with non-small-cell lung cancer (NSCLC) helps clinicians select the best treatment option. Potential NSCLC patients usually undergo invasive tissue biopsy, which may often be unnecessary and delays...

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