High Glucose Accelerates Cell Proliferation and Increases the Secretion and mRNA Expression of Osteopontin in Human Pancreatic Duct Epithelial Cells

Ito, Miho; Makino, Naohiko; Matsuda, Akiko; Ikeda, Yushi; Kakizaki, Yasuharu; Saito, Yoshihiko; Ueno, Yoshiyuki; Kawata, Satoshi

doi:10.3390/ijms18040807

Cited by 21 publications

(19 citation statements)

References 28 publications

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“…There is a 1.5- to 2.0-fold increase in the risk of developing pancreatic cancer in type 2 diabetes mellitus patients [146,147]. The hyperglycemia, which is caused by insulin resistance and inability to suppress inappropriate hepatic glucose release, has been shown to enhance proliferation [148,149], promotes epithelial–mesenchymal transition and cancer stem cells’ properties [150], and metastatic potential in pancreatic cancer [151,152]. Recently, it has been reported that high glucose concentrations in the cell culture medium induce the KRAS G12D mutation in vitro.…”

Section: Pancreatic Cancer and Diabetesmentioning

confidence: 99%

Glucose Metabolism in Pancreatic Cancer

Liang

Raj

Yao

2019

Cancers

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Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and lethal cancers, with a five-year survival rate of around 5% to 8%. To date, very few available drugs have been successfully used to treat PDAC due to the poor understanding of the tumor-specific features. One of the hallmarks of pancreatic cancer cells is the deregulated cellular energetics characterized by the “Warburg effect”. It has been known for decades that cancer cells have a dramatically increased glycolytic flux even in the presence of oxygen and normal mitochondrial function. Glycolytic flux is the central carbon metabolism process in all cells, which not only produces adenosine triphosphate (ATP) but also provides biomass for anabolic processes that support cell proliferation. Expression levels of glucose transporters and rate-limiting enzymes regulate the rate of glycolytic flux. Intermediates that branch out from glycolysis are responsible for redox homeostasis, glycosylation, and biosynthesis. Beyond enhanced glycolytic flux, pancreatic cancer cells activate nutrient salvage pathways, which includes autophagy and micropinocytosis, from which the generated sugars, amino acids, and fatty acids are used to buffer the stresses induced by nutrient deprivation. Further, PDAC is characterized by extensive metabolic crosstalk between tumor cells and cells in the tumor microenvironment (TME). In this review, we will give an overview on recent progresses made in understanding glucose metabolism-related deregulations in PDAC.

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Section: Pancreatic Cancer and Diabetesmentioning

confidence: 99%

Glucose Metabolism in Pancreatic Cancer

Liang

Raj

Yao

2019

Cancers

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“…A meta-analysis has shown that an elevated serum OPN level might be used as a promising diagnostic tool for early identification of PC [ 123 ]. In addition, a recent study has reported that high glucose levels accelerated cell proliferation and increased the secretion of OPN in human pancreatic duct epithelial cells [ 124 ]. However, another study has reported that the presence of OPN in PC might have a protective effect independent of tumor stage [ 125 ], and a recent study has concluded that the relationship between OPN and PC remained unclear [ 126 ].…”

Section: The Association Of Opn With Apoptosis In Inflammatory Gi mentioning

confidence: 99%

Is Osteopontin a Friend or Foe of Cell Apoptosis in Inflammatory Gastrointestinal and Liver Diseases?

Iida

Wagatsuma

Hirayama

et al. 2017

IJMS

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Osteopontin (OPN) is involved in a variety of biological processes, including bone remodeling, innate immunity, acute and chronic inflammation, and cancer. The expression of OPN occurs in various tissues and cells, including intestinal epithelial cells and immune cells such as macrophages, dendritic cells, and T lymphocytes. OPN plays an important role in the efficient development of T helper 1 immune responses and cell survival by inhibiting apoptosis. The association of OPN with apoptosis has been investigated. In this review, we described the role of OPN in inflammatory gastrointestinal and liver diseases, focusing on the association of OPN with apoptosis. OPN changes its association with apoptosis depending on the type of disease and the phase of disease activity, acting as a promoter or a suppressor of inflammation and inflammatory carcinogenesis. It is essential that the roles of OPN in those diseases are elucidated, and treatments based on its mechanism are developed.

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“…In addition to its catabolic role, glucose is used for the synthesis of nucleotides through the pentose phosphate pathway, which is essential to produce ribose for DNA synthesis during cell division. Proliferating cells, such as cancer cells, prefer glucose as fuel to support their rapid proliferation ( Han et al, 2011 ; Jones and Schulze, 2012 ; Ito et al, 2017 ; Luo et al, 2018 ; Zhou et al, 2018 ). For these reasons, it is believed that the media of various cultured cells require high concentrations of glucose to improve cell proliferation.…”

Section: Introductionmentioning

confidence: 99%

Excess Glucose Impedes the Proliferation of Skeletal Muscle Satellite Cells Under Adherent Culture Conditions

Furuichi

Kawabata

Aoki

et al. 2021

Front. Cell Dev. Biol.

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Glucose is a major energy source consumed by proliferating mammalian cells. Therefore, in general, proliferating cells have the preference of high glucose contents in extracellular environment. Here, we showed that high glucose concentrations impede the proliferation of satellite cells, which are muscle-specific stem cells, under adherent culture conditions. We found that the proliferation activity of satellite cells was higher in glucose-free DMEM growth medium (low-glucose medium with a glucose concentration of 2 mM) than in standard glucose DMEM (high-glucose medium with a glucose concentration of 19 mM). Satellite cells cultured in the high-glucose medium showed a decreased population of reserve cells, identified by staining for Pax7 expression, suggesting that glucose concentration affects cell fate determination. In conclusion, glucose is a factor that decides the cell fate of skeletal muscle-specific stem cells. Due to this unique feature of satellite cells, hyperglycemia may negatively affect the regenerative capability of skeletal muscle myofibers and thus facilitate sarcopenia.

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High Glucose Accelerates Cell Proliferation and Increases the Secretion and mRNA Expression of Osteopontin in Human Pancreatic Duct Epithelial Cells

Cited by 21 publications

References 28 publications

Glucose Metabolism in Pancreatic Cancer

Glucose Metabolism in Pancreatic Cancer

Is Osteopontin a Friend or Foe of Cell Apoptosis in Inflammatory Gastrointestinal and Liver Diseases?

Excess Glucose Impedes the Proliferation of Skeletal Muscle Satellite Cells Under Adherent Culture Conditions

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