Background: In the development of several human cancers, it has been established that neutrophil cytosolic factor 2 (NCF2) plays a major part. Therefore, possible functions of NCF2 in ESCC are investigated in this paper.
Methods: The mRNA/protein expression of NCF-2 in ESCC cell lines and tissues were found based on quantitative real-time reverse transcription PCR (qRT-PCR), western blotting, and immunohistochemistry (IHC). A large cohort consisting of 194 postoperative ESCC samples was used for IHC. These data were analyzed based on Chi-square test, Kaplan-Meier analysis, and Cox regression modelling. For the purpose of confirming its role in ESCC cells, we used short hairpin RNA (ShRNA) interfering method to suppress endogenous NCF2 expression.
Results: NCF2 was significantly up-regulated for in ESCC tissues and cell lines in at mRNA and protein levels; and NCF-2 expression was absent for all normal esophageal epithelium detected by IHC. Furthermore, the knockdown of NCF-2 compromised the proliferation and invasion of ESCC cells in vitro.
Conclusion: Positive NCF2 expression in ESCC may facilitate an aggressive phenotype. This may be an independent biomarker in ESCC.
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Elife
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Walter Brendel Center of Experimental Medicine, Biomedical Center, Institute of Cardiovascular Physiology and Pathophysiology, Ludwig-Maximilians-University, Planegg-Martinsried, München, Germany.
S100A8/A9 is an endogenous alarmin secreted by myeloid cells during many acute and chronic inflammatory disorders. Despite increasing evidence of the proinflammatory effects of extracellular S100A8/A9, little is known about its intracellular function. Here, we show that cytosolic S100A8/A9 is indispensable for neutrophil post-arrest modifications during outside-in signaling under flow conditions in vitro and neutrophil recruitment in vivo, independent of its extracellular functions.
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Institute of Molecular and Industrial Biotechnology, Faculty of Biotechnology and Food Sciences, Lodz University of Technology, Stefanowskiego 2/22, 90-537, Lodz, Poland. Electronic address:
The HprSR constitutes the bacterial two-component regulatory system engaged by Escherichia coli to reduce the damaging effects of reactive chlorine and oxygen species present in its cytosol. Hypochlorous acid (HOCl) has been shown to be the molecule capable of activating of the HprSR system. HOCl is produced upon pathogen invasion by phagocytic cells of the human innate immune system, particularly neutrophils, to take advantage of its powerful antimicrobial attributes.
View Article and Find Full Text PDFmBio
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Department of Microbiology and Immunology, College of Medicine, University of Louisville, Louisville, Kentucky, USA.
Unlabelled: species evade degradation and proliferate within alveolar macrophages as an essential step for the manifestation of disease. However, most intracellular bacterial pathogens are restricted in neutrophils, which are the first line of innate immune defense against invading pathogens. Bacterial degradation within neutrophils is mediated by the fusion of microbicidal granules to pathogen-containing phagosomes and the generation of reactive oxygen species (ROS) by the phagocyte NADPH oxidase complex.
View Article and Find Full Text PDFIn Vitro Cell Dev Biol Anim
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Division of Tumor Pathology, NIR-PIT Research Institute, Kansai Medical University, 2-5-1 Shinmachi, Hirakata, Osaka, 573-1010, Japan.
Apoptosis
December 2024
Department of Biochemistry and Molecular Biophysics, Kansas State University, 141 Chalmers Hall, Manhattan, KS, 66506, USA.
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