28P Validation of cytokeratin (CK18) protein expression in epithelial cell lines and in circulating tumor cells (CTCs)

2021 ◽  
Vol 32 ◽  
pp. S1354
Author(s):  
N.V. Raut ◽  
N. Kale ◽  
A. d'Souza ◽  
Y. Patil ◽  
P. Chakraborty ◽  
...  
2001 ◽  
Vol 69 (9) ◽  
pp. 5857-5863 ◽  
Author(s):  
Gerardo Nardone ◽  
Eileen L. Holicky ◽  
James R. Uhl ◽  
Lina Sabatino ◽  
Stefania Staibano ◽  
...  

ABSTRACT Modifications of mucosal phospholipids have been detected in samples from patients with Helicobacter pylori-positive gastritis. These alterations appear secondary to increased phospholipase A2 activity (PLA2). The cytosolic form of this enzyme (cPLA2), normally involved in cellular signaling and growth, has been implicated in cancer pathogenesis. The aim of this study was to investigate cPLA2 expression and PLA2 activity in the gastric mucosae of patients with and without H. pylori infection. In gastric biopsies from 10H. pylori-positive patients, cPLA2 levels, levels of mRNA as determined by reverse transcriptase PCR, levels of protein as determined by immunohistochemistry, and total PLA2 activity were higher than in 10 H. pylori-negative gastritis patients. To clarify whether H. pylori had a direct effect on the cellular expression of cPLA2, we studied cPLA2 expression in vitro with different human epithelial cell lines, one from a patient with larynx carcinoma (i.e., HEp-2 cells) and two from patients with gastric adenocarcinoma (i.e., AGS and MKN 28 cells), incubated with differentH. pylori strains. The levels of cPLA2, mRNA, and protein expression were unchanged in Hep-2 cells independently of cellular adhesion or invasion of the bacteria. Moreover, no change in cPLA2 protein expression was observed in AGS or MKN 28 cells treated with wild-type H. pylori. In conclusion, our study shows increased cPLA2 expression and PLA2activity in the gastric mucosae of patients with H. pyloriinfection and no change in epithelial cell lines exposed to H. pylori.


2019 ◽  
Vol 20 (7) ◽  
pp. 1678 ◽  
Author(s):  
Yi-Chen Lee ◽  
Chun-Yu Lin ◽  
Yen-Hsu Chen ◽  
Wen-Chin Chiu ◽  
Yen-Yun Wang ◽  
...  

Acute lung injury (ALI) is a life-threatening syndrome characterized by acute and severe hypoxemic respiratory failure. Visfatin, which is known as an obesity-related cytokine with pro-inflammatory activities, plays a role in regulation of inflammatory cytokines. The mechanisms of ALI remain unclear in critically ill patients. Survival in ALI patients appear to be influenced by the stress generated by mechanical ventilation and by ALI-associated factors that initiate the inflammatory response. The objective for this study was to understand the mechanisms of how visfatin regulates inflammatory cytokines and promotes ALI. The expression of visfatin was evaluated in ALI patients and mouse sepsis models. Moreover, the underlying mechanisms were investigated using human bronchial epithelial cell lines, BEAS-2B and NL-20. An increase of serum visfatin was discovered in ALI patients compared to normal controls. Results from hematoxylin and eosin (H&E) and immunohistochemistry staining also showed that visfatin protein was upregulated in mouse sepsis models. Moreover, lipopolysaccharide (LPS) induced visfatin expression, activated the STAT3/NFκB pathway, and increased the expression of pro-inflammatory cytokines, including IL1-β, IL-6, and TNF-α in human bronchial epithelial cell lines NL-20 and BEAS-2B. Co-treatment of visfatin inhibitor FK866 reversed the activation of the STAT3/NFκB pathway and the increase of pro-inflammatory cytokines induced by LPS. Our study provides new evidence for the involvement of visfatin and down-stream events in acute lung injury. Further studies are required to confirm whether the anti-visfatin approaches can improve ALI patient survival by alleviating the pro-inflammatory process.


2003 ◽  
Vol 80 (4) ◽  
pp. 444-450 ◽  
Author(s):  
Jae-Kyung Myung ◽  
Kurt Krapfenbauer ◽  
Rachel Weitzdoerfer ◽  
Andreas Peyrl ◽  
Michael Fountoulakis ◽  
...  

2007 ◽  
Vol 4 (1) ◽  
pp. 11 ◽  
Author(s):  
Joanna Szmydynger-Chodobska ◽  
Crissey L Pascale ◽  
Andrew N Pfeffer ◽  
Cassaundra Coulter ◽  
Adam Chodobski

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