Identification of proteins implicated in the development of pancreatic cancer-associated diabetes mellitus by iTRAQ-based quantitative proteomics

Wang, Wansheng; Liu, Xiaohui; Liu, Lingxiao; Jin, Dong-Yan; Yang, Pengyuan; Wang, Xiaolin

doi:10.1016/j.jprot.2013.03.031

Cited by 23 publications

(11 citation statements)

References 32 publications

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“…Numerous genes were found to be differentially expressed on bioinformatic analysis of the gene expression profiles, consistent with former reports [16,17]. We then extracted secretory genes and did GO analysis.…”

Section: Discussionsupporting

confidence: 86%

Analysis of global gene expression profiles suggests a role of acute inflammation in type 3C diabetes mellitus caused by pancreatic ductal adenocarcinoma

Gao

Zhou

et al. 2015

Diabetologia

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Aims/hypothesis Pancreatic ductal adenocarcinoma (PDAC) can cause type 3C diabetes, known as PDAC-associated diabetes mellitus (PDAC-DM), but the mechanism is unknown. This study aimed to reveal the mechanism. Methods PDAC lesions from patients with or without PDAC-DM (n=4 in each group) were individually profiled for 23,512 mRNAs with microarrays. Bioinformatic analysis and in vivo and in vitro assays were then conducted. Results We determined that 2,778 genes were differentially expressed; over-representation of ten genes was validated with quantitative RT-PCR. The analysis of gene ontology showed that the differentially expressed secretory genes were related mainly to inflammation. High levels of a marker of inflammation (C-reactive protein [CRP]) and an inflammatory mediator (TNF super-family member 13 [TNFSF13]) were found in the serum of patients with PDAC-DM. After surgical resection of PDAC lesions, CRP and TNFSF13 levels significantly decreased (p<0.01). Furthermore, we found that the levels of TNFSF13 in PDAC lesions and TNFSF13 and CRP in serum were significantly correlated with the diabetic status of patients with PDAC-DM (p<0.01). Assays in vivo showed that after exposure to an inhibitor of inflammation (celecoxib), the fasting blood glucose level in the mouse model of PDACWenchao Gao, Yu Zhou and Qingyan Li contributed equally to this work Electronic supplementary material The online version of this article

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Section: Discussionsupporting

confidence: 86%

Analysis of global gene expression profiles suggests a role of acute inflammation in type 3C diabetes mellitus caused by pancreatic ductal adenocarcinoma

Gao

Zhou

et al. 2015

Diabetologia

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“…111 Another proteomic study found upregulation of S100-A9 in pancreatic ductal adenocarcinoma tissues with diabetes compared with those without diabetes. 112 S100A8/A9 is highly abundant in neutrophils and activated monocytes or macrophages, and these findings might reflect the myeloid cell infiltration observed even at early stages of pancreatic ductal adenocarcinoma development. 113,114 A study using peripheral blood mononuclear cell gene profiling for pancreatic ductal adenocarcinoma proposed vanin-1 and matrix metalloproteinase-9 (MMP9) as biomarkers to discriminate diabetes secondary to pancreatic cancer from type 2 diabetes.…”

Section: Diabetes Secondary To Pancreatic Cancermentioning

confidence: 93%

Type 3c (pancreatogenic) diabetes mellitus secondary to chronic pancreatitis and pancreatic cancer

Hart

Bellin

Andersen

et al. 2016

The Lancet Gastroenterology & Hepatology

338

286

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Diabetes mellitus is a group of diseases defined by persistent hyperglycaemia. Type 2 diabetes, the most prevalent form, is characterised initially by impaired insulin sensitivity and subsequently by an inadequate compensatory insulin response. Diabetes can also develop as a direct consequence of other diseases, including diseases of the exocrine pancreas. Historically, diabetes due to diseases of the exocrine pancreas was described as pancreatogenic or pancreatogenous diabetes mellitus, but recent literature refers to it as type 3c diabetes. It is important to note that type 3c diabetes is not a single entity; it occurs because of a variety of exocrine pancreatic diseases with varying mechanisms of hyperglycaemia. The most commonly identified causes of type 3c diabetes are chronic pancreatitis, pancreatic ductal adenocarcinoma, haemochromatosis, cystic fibrosis, and previous pancreatic surgery. In this Review, we discuss the epidemiology, pathogenesis, and clinical relevance of type 3c diabetes secondary to chronic pancreatitis and pancreatic ductal adenocarcinoma, and highlight several important knowledge gaps.

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“…Source: extracted from Suppl. Tables S3 and S4 of Wang et al (2013a), including proteins with >3/2 or <2/3 fold change in at least 3 of 4 iTRAQ experiments for different pooled samples. LCM of CD24 + cells from PDAC vs CD24 − cells from adjacent normal tissue (ANT).…”

Section: Data Sourcesmentioning

confidence: 99%

“…1B show that up-expressed proteins in pancreatic cancer often have significantly higher Z C [ ]. A dataset obtained for pancreatic cancer associated with diabetes mellitus (Wang et al, 2013a) [ ] has both significantly higher Z C and n H 2 O . Only one dataset, from a study that targeted accessible proteins (Turtoi et al, 2011) (Chen et al, 2007), accessible proteins (Turtoi et al, 2011), and low-grade tumors (Wang et al, 2013b).…”

Section: /24mentioning

confidence: 99%

Chemical composition and the potential for proteomic transformation in cancer, hypoxia, and hyperosmotic stress

Dick¹

2017

Preprint

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Models of chemical composition and thermodynamic potential emphasize the microenvironmental context for proteomic transformations. Here, data from 71 comparative proteomics studies were analyzed using elemental ratios and chemical components as measures of oxidation and hydration state. Experimental lowering of oxygen availability (hypoxia) and water activity (hyperosmotic stress) are reflected in decreased oxidation and hydration states of proteomes, but up-expressed proteins in colorectal and pancreatic cancer most often have higher average oxidation or hydration state. Calculations of chemical affinity were used to quantify the thermodynamic potentials for transformation of proteomes as a function of fugacity of O 2 and activity of H 2 O, which serve as scales of oxidation and hydration potential. Potential diagrams for the overall reactions between down-and up-expressed proteins in various datasets have predicted equipotential lines that cluster near unit activity of H 2 O, suggesting that protein expression is sensitive to local variations in water activity. A redox balance calculation indicates that an increase in the lipid to protein ratio in cancer cells by 20% over hypoxic cells would generate an electron sink of sufficient size for oxidation of the cancer proteomes. These findings demonstrate consistent, condition-dependent chemical differences between proteomes, identify primary microenvironmental constraints on proteomic transformations, and help to quantify the redox balance among cellular macromolecules. The datasets and computer code used here are supplied in a new R package, canprot.

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Identification of proteins implicated in the development of pancreatic cancer-associated diabetes mellitus by iTRAQ-based quantitative proteomics

Cited by 23 publications

References 32 publications

Analysis of global gene expression profiles suggests a role of acute inflammation in type 3C diabetes mellitus caused by pancreatic ductal adenocarcinoma

Analysis of global gene expression profiles suggests a role of acute inflammation in type 3C diabetes mellitus caused by pancreatic ductal adenocarcinoma

Type 3c (pancreatogenic) diabetes mellitus secondary to chronic pancreatitis and pancreatic cancer

Chemical composition and the potential for proteomic transformation in cancer, hypoxia, and hyperosmotic stress

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