Activation of the receptor for glycation end products (RAGE) by its ligands in pancreatic cancer cells

Kadasah, Sultan; Thiyagarajan, Swetha; Vetter, Stefan; Leclerc, Estelle

doi:10.1096/fasebj.2019.33.1_supplement.476.11

Cited by 2 publications

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“…For example, NF-κB activation represents a signaling event engaged in response to various RAGE ligands, as it has been demonstrated for AGEs, HMGB-1, several S100 proteins, and HSP70. For instance, the binding of RAGE by its ligands AGEs, S100P and S100A8/A9 induced transcriptional effects and biological responses dependent on NF-κB activation in pancreatic cancer cells ( 219 ). In addition, extracellular HSP70 binds RAGE to trigger NF-κB proinflammatory gene expression in human lung cancer cells ( 220 ).…”

Section: Rage and Iigfs Cross-talk In Meta-inflammationmentioning

confidence: 99%

Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy

et al. 2023

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In metabolic conditions such as obesity and diabetes, which are associated with deregulated signaling of the Insulin/IGF system (IIGFs), inflammation plays a dominant role. In cancer, IIGFs is implicated in disease progression, particularly during obesity and diabetes, however further mediators may act in concert with IIGFs to trigger meta-inflammation. The receptor for advanced glycation end-products (RAGE) and its ligands bridge together metabolism and inflammation in obesity, diabetes and cancer. Herein, we summarize the main mechanisms of meta-inflammation in malignancies associated with obesity and diabetes; we provide our readers with the most recent understanding and conceptual advances on the role of RAGE at the crossroad between impaired metabolism and inflammation, toward disease aggressiveness. We inform on the potential hubs of cross-communications driven by aberrant RAGE axis and dysfunctional IIGFs in the tumor microenvironment. Furthermore, we offer a rationalized view on the opportunity to terminate meta-inflammation via targeting RAGE pathway, and on the possibility to shut its molecular connections with IIGFs, toward a better control of diabetes- and obesity-associated cancers.

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Section: Rage and Iigfs Cross-talk In Meta-inflammationmentioning

confidence: 99%

Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy

et al. 2023

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Neuroendocrine and Behavioral Consequences of Hyperglycemia in Cancer

Vasquez

Borniger

2020

Endocrinology

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A hallmark of cancer is the disruption of cellular metabolism during the course of malignant growth. Major focus is now on how these cell-autonomous processes propagate to the tumor microenvironment and, more generally, to the entire host system. This chain of events can have major consequences for a patient’s health and wellbeing. For example, metabolic “waste” produced by cancer cells activates systemic inflammatory responses, which can interfere with hepatic insulin receptor signaling and glucose homeostasis. Research is just now beginning to understand how these processes occur, and how they contribute to systemic symptoms prevalent across cancers, including hyperglycemia, fatigue, pain, and sleep disruption. Indeed, it is only recently that we have begun to appreciate that the brain does not play a passive role in responding to cancer-induced changes in physiology. In this review, we provide a brief discussion of how oncogene-directed metabolic reprogramming disrupts host metabolism, with a specific emphasis on cancer-induced hyperglycemia. We further discuss how the brain senses circulating glucose concentrations and how this process goes awry as a response to distant neoplastic growth. Finally, as glucose-sensing neurons control diverse aspects of physiology and behavior, we link cancer-induced changes in energy balance to neuroendocrine and behavioral consequences for the host organism.

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Activation of the receptor for glycation end products (RAGE) by its ligands in pancreatic cancer cells

Cited by 2 publications

References 0 publications

Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy

Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy

Neuroendocrine and Behavioral Consequences of Hyperglycemia in Cancer

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