Promotion of anoxia‑reoxygenation‑induced inflammation and permeability enhancement by nicotinamide phosphoribosyltransferase‑activated MAPK signaling in human umbilical vein endothelial cells

Yan, Nao; Yang, Wei; Dong, Xiao; Qiao, Fang; Gong, Yi; Zhou, Jianuan; Xu, Jianjun

doi:10.3892/etm.2017.5083

Cited by 2 publications

(2 citation statements)

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“…NAMPT has been reported to activate MAPK signaling. As per our results, MAPK signaling was synergistically upregulated with NAMPT expression . In addition, NAMPT has also been associated with chronic inflammation in pancreatic cancer and is thought to contribute to drug resistance .…”

Section: Discussionsupporting

confidence: 85%

Screening common signaling pathways associated with drug resistance in non‐small cell lung cancer via gene expression profile analysis

et al. 2019

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Lung cancer is the leading cause of cancer‐related deaths worldwide. Although several therapeutic strategies have been employed to curb lung cancer, the survival rate is still poor owing to the development of drug resistance. The mechanisms underlying drug resistance development are incompletely understood. Here, we aimed to identify the common signaling pathways involved in drug resistance in non‐small cell lung cancer (NSCLC). Three published transcriptome microarray data were downloaded from the Gene Expression Omnibus (GEO) database comprising different drug‐resistant cell lines and their parental cell lines. Differentially expressed genes (DEGs) were identified and used to perform Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. An overlapping analysis was performed for KEGG pathways enriched from all the three datasets to identify the common signaling pathways. As a result, we found that metabolic pathways, ubiquitin‐mediated proteolysis, and mitogen‐activated protein kinase (MAPK) signaling were the most aberrantly expressed signaling pathways. The knockdown of nicotinamide phosphoribosyltransferase (NAMPT), the gene involved in metabolic pathways and known to be upregulated in drug‐resistant tumor cells, was shown to increase the apoptosis of cisplatin‐resistant A549 cells following cisplatin treatment. Thus, our results provide an in‐depth analysis of the signaling pathways that are commonly altered in drug‐resistant NSCLC cell lines and highlight the potential strategy that facilitates the development of interventions to interfere with upregulated signaling pathways as well as to boost downregulated signaling pathways in drug‐resistant tumors for the elimination of multiple resistance of NSCLC.

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Section: Discussionsupporting

confidence: 85%

Screening common signaling pathways associated with drug resistance in non‐small cell lung cancer via gene expression profile analysis

et al. 2019

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“…Cell permeability increases, and adenovirus-encoding sh-PBEF can reduce the changes in permeability 25 through the MAPK and ERK signaling pathways. 26 In addition, PBEF could inhibit sodium–water transport system-related protein expression in rat type I and type II alveolar epithelial cells. 8 , 27…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Pre-B Cell Colony Enhancing Factor Reduces Lung Injury in Rats Receiving Cardiopulmonary Bypass

Lü

Yang

Zhou

et al. 2021

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Objective: Pre-B cell colony enhancing factor (PBEF) is an important proinflammatory cytokine involved in acute lung injury. However, whether PBEF participates in lung injury caused by cardiopulmonary bypass (CPB) is still unknown. This study aimed to investigate the effects of silencing PBEF on lung injury and the sodium and water transport system in rats receiving CPB. Methods: Morphological changes in lung tissues were evaluated using hematoxylin and eosin (H&E) staining. PBEF was detected using immunohistochemistry. The sodium and water transport system-related proteins and cellular signaling pathways were detected by Western blotting. Results: Rats receiving CPB (model group) had more severe alveolar wall damage and higher expression of PBEF in free form than the control rats. Western blotting showed that the expression of PBEF, surfactant protein D (SP), aquaporin (AQP) 1, AQP5, and epithelial sodium channel (ENaC) was significantly higher in the lung tissue of CPB rats than control rats. By contrast, adenovirus-encoding sh-PBEF significantly reduced the expression of PBEF, SP, AQP1, AQP5, and ENaC in the lung tissues of rats treated with CPB. The phosphorylation levels of extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), protein kinase B (AKT), and p38 mitogen-activated protein kinase (MAPK) were significantly increased in the lung tissue of rats that received CPB, and were downregulated by adenovirus-encoding sh-PBEF. Conclusion: Adenovirus-encoding sh-PBEF could reduce lung injury and repair the sodium-water transport system in rats receiving CPB, likely through reducing MAPK, ERK1/2, and Akt signaling pathways.

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Promotion of anoxia‑reoxygenation‑induced inflammation and permeability enhancement by nicotinamide phosphoribosyltransferase‑activated MAPK signaling in human umbilical vein endothelial cells

Cited by 2 publications

References 32 publications

Screening common signaling pathways associated with drug resistance in non‐small cell lung cancer via gene expression profile analysis

Screening common signaling pathways associated with drug resistance in non‐small cell lung cancer via gene expression profile analysis

Inhibition of Pre-B Cell Colony Enhancing Factor Reduces Lung Injury in Rats Receiving Cardiopulmonary Bypass

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