scholarly journals Quantitative proteomics analysis of the role of tetraspanin-8 in the drug resistance of gastric cancer

2017 ◽  
Author(s):  
Lan Li ◽  
Daping Yang ◽  
Dejun Cui ◽  
Yu Li ◽  
Zhao Nie ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Quantitative Proteomics ◽  
Proteomics Analysis

scholarly journals Comparative Proteomics Analysis of Mouse Habu Nephritis Models with and without Unilateral Nephrectomy

2016 ◽  
Vol 39 (5) ◽  
pp. 1761-1776 ◽  
Author(s):  
Lei Chen ◽  
Yang Lu ◽  
Jun Wen ◽  
Xu Wang ◽  
Lingling Wu ◽  
...  
Keyword(s):  
Renal Injury ◽  
Quantitative Proteomics ◽  
Mesangial Cells ◽  
Unilateral Nephrectomy ◽  
Label Free ◽  
Proteomics Analysis ◽  
Single Kidney ◽  
Regulation Of Actin Cytoskeleton ◽  
Insight Into

Background/Aims: Individuals possessing a single kidney are at greater risk of renal injury upon exposure to harmful stimuli. This study aimed to explore the pathogenesis of renal injury in glomerulonephritis with versus without unilateral nephrectomy (UNX). Methods: Histological analysis and label-free quantitative proteomics were performed on two models—the Habu snake venom-induced glomerulonephritis model with versus without UNX (HabuU and Habu models, respectively). The role of villin 1, a differentially expressed protein (DEP) in mouse mesangial cells, was investigated. Results: Persistent mesangiolysis and focal hypercellularity together with reduced activation of cell proliferation in the HabuU model induced more serious renal injury compared with that in the Habu model. The DEPs between the two models were identified by label-free liquid chromatography-mass spectrometry. The KEGG pathway results indicated that regulation of actin cytoskeleton and focal adhesion were specifically enriched in the HabuU model. The cytoskeleton regulation protein villin 1 was downregulated in the HabuU model, but unchanged in the Habu model. Knockdown of villin 1 promoted apoptosis and inhibited the proliferation of mouse mesangial cells, suggesting villin 1 to be involved in qlomerular lesion self-repair insufficiency. Conclusion: By assessing the proteomic profiles of the two models, this study identified several important differences, particularly villin 1 expression, in regulatory mechanisms between the two models. Our findings provide novel insight into the mechanism of serious renal injury in glomerulonephritis with UNX.

scholarly journals The Role of Autophagy in Gastric Cancer Chemoresistance: Friend or Foe?

2020 ◽  
Vol 8 ◽  
Author(s):  
Jing-Li Xu ◽  
Li Yuan ◽  
Yan-Cheng Tang ◽  
Zhi-Yuan Xu ◽  
Han-Dong Xu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Molecular Mechanisms ◽  
Chemotherapy Resistance ◽  
Dual Roles ◽  
Non Coding Rnas ◽  
Regulatory Effects ◽  
Cancer Chemoresistance ◽  
The Relationship

Gastric cancer is the third most common cause of cancer-related death worldwide. Drug resistance is the main inevitable and vital factor leading to a low 5-year survival rate for patients with gastric cancer. Autophagy, as a highly conserved homeostatic pathway, is mainly regulated by different proteins and non-coding RNAs (ncRNAs) and plays dual roles in drug resistance of gastric cancer. Thus, targeting key regulatory nodes in the process of autophagy by small molecule inhibitors or activators has become one of the most promising strategies for the treatment of gastric cancer in recent years. In this review, we provide a systematic summary focusing on the relationship between autophagy and chemotherapy resistance in gastric cancer. We comprehensively discuss the roles and molecular mechanisms of multiple proteins and the emerging ncRNAs including miRNAs and lncRNAs in the regulation of autophagy pathways and gastric cancer chemoresistance. We also summarize the regulatory effects of autophagy inhibitor and activators on gastric cancer chemoresistance. Understanding the vital roles of autophagy in gastric cancer chemoresistance will provide novel opportunities to develop promising therapeutic strategies for gastric cancer.

scholarly journals Quantitative proteomics analysis of Mycoplasma pneumoniae identifies potential macrolide resistance determinants

2020 ◽  
Author(s):  
shaoli li ◽  
guanhua xue ◽  
hanqing zhao ◽  
yanling feng ◽  
chao yan ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Mycoplasma Pneumoniae ◽  
Quantitative Proteomics ◽  
Molecular Mechanisms ◽  
Resistance Mechanisms ◽  
Community Acquired Pneumonia ◽  
Proteomics Analysis ◽  
Tandem Mass Tag ◽  
Peptide Biosynthesis ◽  
Resistant Strains

Abstract Mycoplasma pneumoniae is one of the leading causes of community-acquired pneumonia in children and adolescents. Because of the wide application of macrolides in clinical treatment, macrolide-resistant M. pneumoniae strains have become increasingly common worldwide. However, the molecular mechanisms underlying drug resistance in M. pneumoniae are poorly understood. In the present work, we analyzed the whole proteomes of macrolide-sensitive and macrolide-resistant strains of M. pneumoniae using a tandem mass tag-labeling quantitative proteomic technique, Data are available via ProteomeXchange with identifier PXD022220. In total, 165 differentially expressed proteins were identified, of which 80 were upregulated and 85 were downregulated in the drug-resistant strain compared with the sensitive strain. Functional analysis revealed that these proteins were predominantly involved in protein and peptide biosynthesis processes, the ribosome, and transmembrane transporter activity, which implicates them in the mechanism(s) of resistance of M. pneumoniae to macrolides. Our results provide new insights into drug resistance in M. pneumoniae and identify potential targets for further studies on resistance mechanisms in this bacterium.

scholarly journals Bacterioferritin: a key iron storage modulator that affects strain growth and butenyl-spinosyn biosynthesis in Saccharopolyspora pogona

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Jianli Tang ◽  
Zirong Zhu ◽  
Haocheng He ◽  
Zhudong Liu ◽  
Ziyuan Xia ◽  
...  
Keyword(s):  
Stress Resistance ◽  
Quantitative Proteomics ◽  
Polyketide Synthase ◽  
Storage Capacity ◽  
Oxidative Stress Response ◽  
Iron Toxicity ◽  
Intracellular Iron ◽  
Proteomics Analysis ◽  
Iron Storage

Abstract Background Butenyl-spinosyn, produced by Saccharopolyspora pogona, is a promising biopesticide due to excellent insecticidal activity and broad pesticidal spectrum. Bacterioferritin (Bfr, encoded by bfr) regulates the storage and utilization of iron, which is essential for the growth and metabolism of microorganisms. However, the effect of Bfr on the growth and butenyl-spinosyn biosynthesis in S. pogona has not been explored. Results Here, we found that the storage of intracellular iron influenced butenyl-spinosyn biosynthesis and the stress resistance of S. pogona, which was regulated by Bfr. The overexpression of bfr increased the production of butenyl-spinosyn by 3.14-fold and enhanced the tolerance of S. pogona to iron toxicity and oxidative damage, while the knockout of bfr had the opposite effects. Based on the quantitative proteomics analysis and experimental verification, the inner mechanism of these phenomena was explored. Overexpression of bfr enhanced the iron storage capacity of the strain, which activated polyketide synthase genes and enhanced the supply of acyl-CoA precursors to improve butenyl-spinosyn biosynthesis. In addition, it induced the oxidative stress response to improve the stress resistance of S. pogona. Conclusion Our work reveals the role of Bfr in increasing the yield of butenyl-spinosyn and enhancing the stress resistance of S. pogona, and provides insights into its enhancement on secondary metabolism, which provides a reference for optimizing the production of secondary metabolites in actinomycetes.

scholarly journals Quantitative proteomics analysis of Mycoplasma pneumoniae identifies potential macrolide resistance determinants

AMB Express ◽  
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Shaoli Li ◽  
Guanhua Xue ◽  
Hanqing Zhao ◽  
Yanling Feng ◽  
Chao Yan ◽  
...  
Keyword(s):  
Drug Resistance ◽  
Mycoplasma Pneumoniae ◽  
Quantitative Proteomics ◽  
Molecular Mechanisms ◽  
Resistance Mechanisms ◽  
Community Acquired Pneumonia ◽  
Proteomics Analysis ◽  
Tandem Mass Tag ◽  
Peptide Biosynthesis ◽  
Resistant Strains

AbstractMycoplasma pneumoniae is one of the leading causes of community-acquired pneumonia in children and adolescents. Because of the wide application of macrolides in clinical treatment, macrolide-resistant M. pneumoniae strains have become increasingly common worldwide. However, the molecular mechanisms underlying drug resistance in M. pneumoniae are poorly understood. In the present work, we analyzed the whole proteomes of macrolide-sensitive and macrolide-resistant strains of M. pneumoniae using a tandem mass tag-labeling quantitative proteomic technique, Data are available via ProteomeXchange with identifier PXD022220. In total, 165 differentially expressed proteins were identified, of which 80 were upregulated and 85 were downregulated in the drug-resistant strain compared with the sensitive strain. Functional analysis revealed that these proteins were predominantly involved in protein and peptide biosynthesis processes, the ribosome, and transmembrane transporter activity, which implicates them in the mechanism(s) of resistance of M. pneumoniae to macrolides. Our results provide new insights into drug resistance in M. pneumoniae and identify potential targets for further studies on resistance mechanisms in this bacterium.

scholarly journals Emerging Role of miRNAs in the Drug Resistance of Gastric Cancer

2016 ◽  
Vol 17 (3) ◽  
pp. 424 ◽  
Author(s):  
Ismael Riquelme ◽  
Pablo Letelier ◽  
Angela Riffo-Campos ◽  
Priscilla Brebi ◽  
Juan Roa
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance

scholarly journals Role of Ss-A/Ro ribonucleoprotein 60 ku subunit variant 1 in multi-drug resistance of gastric cancer

2008 ◽  
Vol 16 (8) ◽  
pp. 814
Author(s):  
Quan-Li Han ◽  
Long-Fang Zhang ◽  
Xi-Dong Zhang ◽  
Xiao-Wei Jin ◽  
Ling Yang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Drug Resistance ◽  
Multi Drug Resistance ◽  
Ro Ribonucleoprotein

Quantitative Proteomics Analysis Revealed the Potential Role of lncRNA Ftx in Promoting Aortic Dissection Progression

2021 ◽  
Author(s):  
Xiangfei Sun ◽  
Junyong Zhang ◽  
Qingbao Li ◽  
Qi Zhao ◽  
Rui Chen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Endothelial Cells ◽  
Aortic Dissection ◽  
Quantitative Proteomics ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Biological Processes ◽  
Cell Models ◽  
Proliferation And Apoptosis

Abstract Objective: The destruction of vascular endothelial function is an important mechanism for the formation of aortic dissection. Here, we aim to investigate the role of lncRNA Ftx in the biological functions of vascular endothelial cells, as well as the key proteins it regulates, to further explore the potential regulatory role of Ftx on the function of vascular endothelial cells in the pathogenesis of aortic dissection.Experimental Design: The expression of lncRNA Ftx was measured in aortic dissection tissues（n＝12）and age- and sex-matched patients with hypertension tissues（n＝12）. Loss and Gain-of-Function cell Models was constructed using the lentivirus mediated Ftx/Sh-Ftx transfection in HUVECs. The quantitative proteomics was performed to profile the differentially expressed proteins in cell models and further defined the crucial molecules and pathways involved in the carcinogenesis process of lncRNA Ftx. Cell experiments was conducted for valuable proteins to verify the regulatory effect by Ftx.Results: The results of clinical specimen examination showed that LncRNA Ftx was significantly over-expressed in aortic dissection tissue compared with normal aortic tissue. A total of 4348 proteins were quantified by protein mass spectrometry, which are involved in various biological processes and related signaling pathways including cell proliferation, cell apoptosis, cell functional changes and cell metabolism. Interestingly,CBX1, is a protein associated with proliferation and apoptosis of vascular endothelial cells,was up-regulated in the absence of LncRNA Ftx and down-regulated in the overexpression of LncRNA Ftx, which was further verified in HUVECs. Conclusion: This study showed that the intervention of LncRNA Ftx expression in vascular endothelial cells can regulate multiple biological processes such as cell proliferation and apoptosis, thus affecting the progression of aortic dissection. In this process, LncRNA Ftx may have a negative regulation effect on CBX1. which provided a new perspective for the mechanism of gastric cancer progression, and thus identified potential therapeutic targets for gastric cancer.

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