Advanced Glycation End-Products: A Biological Consequence of Lifestyle Contributing to Cancer Disparity

Turner, David P.

doi:10.1158/0008-5472.can-15-0169

Cited by 86 publications

(62 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It is reported that dietary consumption of AGEs rich foods led to increasing circulating AGEs level [3,4]. Then, these AGEs in circulation might be able to react with lung cancer cells.…”

Section: Discussionmentioning

confidence: 99%

“…It is reported that the intake of foods rich in AGEs increased AGEs content in circulation of patients with diabetes or chronic kidney disease [2,3]. So far, the impact of AGEs upon cancer progression has attracted more attention because AGE level in tumors was markedly increased [4]. It is indicated that AGEs could engage with their receptor (RAGE), and the engagement in turn enhanced RAGE protein expression, and activated p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B (NF-κB) signaling pathways [5].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Carboxymethyllysine, an Advanced Glycation End-Product, Promotes the Invasion and Migration of Lung Cancer A549 Cells

Hsia¹

2017

CMR

View full text Add to dashboard Cite

Effects of carboxymethyllysine (CML), an advanced glycation end-product (AGE), at 1, 2, 4, 8 or 16 µmol/l upon invasion and migration of A549 cells, non-small cell lung cancer (NSCLC) cells, were investigated. Results showed that CML at used test doses did not affect A549 cell growth. However, CML at 4-16 µmol/l enhanced both invasion and migration, and stimulated the release of reactive oxygen species, interleukin-6 and tumor necrosis factor-alpha in A549 cells. CML at 2-16 µmol/l increased protein expression of AGE receptor, p47 phox , intercellular adhesion molecule-1, fibronectin, kappa-B (NF-κB) p65 and p-p38 in A549 cells. CML only at 4-16 µmol/l increased matrix metalloproteinase-2 expression in A549 cells. These findings indicated that CML might benefit NSCLC metastasis through promoting invasion and migration.

show abstract

“…It is reported that dietary consumption of AGEs rich foods led to increasing circulating AGEs level [3,4]. Then, these AGEs in circulation might be able to react with lung cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Carboxymethyllysine, an Advanced Glycation End-Product, Promotes the Invasion and Migration of Lung Cancer A549 Cells

Hsia¹

2017

CMR

View full text Add to dashboard Cite

show abstract

“…These observations, however, conflict with the well-known pathogenic actions of AGEs [52]. Because biological AGE levels vary among different populations [25], the aforementioned findings need to be confirmed in other populations. Notably, higher plasma CML levels are positively associated with the risk of prostate cancer [51], and AGE-related plasma fluorescence may be inversely associated with the prognosis of lung cancer [49].…”

Section: Epidemiological and Animal Studymentioning

confidence: 94%

Glycative stress from advanced glycation end products (AGEs) and dicarbonyls: An emerging biological factor in cancer onset and progression

Lin

et al. 2016

Molecular Nutrition Food Res

View full text Add to dashboard Cite

In recent years, glycative stress from exogenous or endogenous advanced glycation end products (AGEs) and highly reactive dicarbonyls has gained great attention for its putative effects on cancer development. AGEs are a group of compounds formed from the complex chemical reaction of reducing sugars with compounds containing an amino group. AGEs bind to and activate the receptor for AGEs (RAGE), which is a predominant modulator of inflammation-associated cancer, and AGEs induce reactive oxygen species that are an important regulator of the hallmarks of cancer. Dicarbonyls, which are formed during glycolysis, lipid oxidation, or protein degradation, include glyoxal, methylglyoxal, and 3-deoxyglucosone and are regarded as major precursors of AGEs. These dicarbonyls not only fuel the AGE pool in living organisms but also evoke carbonyl stress, which may contribute to the carbonylative damage of carbohydrates, lipids, proteins, or DNA. Carbonylative damage then leads to many lesions, some of which are implicated in the pathogenesis of cancer. In this review, studies regarding the effects of AGEs and dicarbonyls on cancer onset or progression are systematically discussed, and the utilization of AGE inhibitors and dicarbonyl scavengers in cancer therapy are noted.

show abstract

“…Further studies on the efficacy of phytochemicals to reverse hypomethylation‐induced genetic aberrations are needed. Advanced glycation end‐products (AGE) resulting from nonenzymatic glycation are associated with increased risk and progression of BC . Exogenous AGE treatment leads to stimulation of BC cell proliferation, migration and invasion .…”

Section: Determinants Of Bc Risk: Considerations For Bc Prevention Anmentioning

confidence: 99%

Translational opportunities for broad‐spectrum natural phytochemicals and targeted agent combinations in breast cancer

Nagaprashantha

Adhikari

Singhal

et al. 2017

Intl Journal of Cancer

View full text Add to dashboard Cite

Breast cancer (BC) prevention and therapy in the context of life-style risk factors and biological drivers is a major focus of developmental therapeutics in oncology. Obesity, alcohol, chronic estrogen signaling and smoking have distinct BC precipitating and facilitating effects that may act alone or in combination. A spectrum of signaling events including enhanced oxidative stress and changes in estrogen-receptor (ER)-dependent and -independent signaling drive the progression of BC. Breast tumors modulate ERα/ERβ ratio, upregulate proliferative pathways driven by ERα and HER2 with a parallel loss and/or downregulation of tumor suppressors such as TP53 and PTEN which together impact the efficacy of therapeutic strategies and frequently lead to emergence of drug resistance. Natural phytochemicals modulate oxidative stress, leptin, integrin, HER2, MAPK, ERK, Wnt/β-catenin and NFκB signaling along with regulating ERα and ERβ, thereby presenting unique opportunities for both primary and combinatorial interventions in BC. In this regard, this article focuses on critical analyses of the evidence from multiple studies on the efficacy of natural phytochemicals in BC. In addition, areas in which the combinations of such effective natural phytochemicals with approved and/or developing anticancer agents can be translationally beneficial are discussed to derive evidence-based inference for addressing challenges in BC control and therapy.

show abstract

Advanced Glycation End-Products: A Biological Consequence of Lifestyle Contributing to Cancer Disparity

Cited by 86 publications

References 31 publications

Carboxymethyllysine, an Advanced Glycation End-Product, Promotes the Invasion and Migration of Lung Cancer A549 Cells

Carboxymethyllysine, an Advanced Glycation End-Product, Promotes the Invasion and Migration of Lung Cancer A549 Cells

Glycative stress from advanced glycation end products (AGEs) and dicarbonyls: An emerging biological factor in cancer onset and progression

Translational opportunities for broad‐spectrum natural phytochemicals and targeted agent combinations in breast cancer

Contact Info

Product

Resources

About