Ketohexokinase-A acts as a nuclear protein kinase that mediates fructose-induced metastasis in breast cancer

Kim, Jiyoung; Kang, Ji Yeon; Kang, Ye Lim; Woo, Jongmin Jacob; Kim, Youngsoo; Huh, June; Park, Jong-Wan

doi:10.1038/s41467-020-19263-1

Cited by 50 publications

(38 citation statements)

References 44 publications

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“…In humans, the conversion of fructose via KHK is assumed to be mainly restricted to liver [46,47]. However, in tumors, KHK is apparently expressed more frequently [48][49][50]. To our knowledge, there is no experimental evidence that this pathway is physiologically relevant.…”

Section: Polyol Pathwaymentioning

confidence: 99%

Fructose Metabolism in Cancer

Krause

Wegner

2020

Cells

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The interest in fructose metabolism is based on the observation that an increased dietary fructose consumption leads to an increased risk of obesity and metabolic syndrome. In particular, obesity is a known risk factor to develop many types of cancer and there is clinical and experimental evidence that an increased fructose intake promotes cancer growth. The precise mechanism, however, in which fructose induces tumor growth is still not fully understood. In this article, we present an overview of the metabolic pathways that utilize fructose and how fructose metabolism can sustain cancer cell proliferation. Although the degradation of fructose shares many of the enzymes and metabolic intermediates with glucose metabolism through glycolysis, glucose and fructose are metabolized differently. We describe the different metabolic fates of fructose carbons and how they are connected to lipogenesis and nucleotide synthesis. In addition, we discuss how the endogenous production of fructose from glucose via the polyol pathway can be beneficial for cancer cells.

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Section: Polyol Pathwaymentioning

confidence: 99%

Fructose Metabolism in Cancer

Krause

Wegner

2020

Cells

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“…In addition to dietary restriction, many studies have investigated enzymatic alterations of fructose metabolism in cancer. While the inborn error of KHK deficiency was described as not causing adverse effects, it has been found that in breast cancer, fructose intake induces KHK-A (ubiquitously expressed KHK isoform) entrance into the nucleus, leading to a signaling cascade triggering the metastatic phenotype [ 68 ].…”

Section: Fructose Metabolism Disordersmentioning

confidence: 99%

Fructose and Mannose in Inborn Errors of Metabolism and Cancer

et al. 2021

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History suggests that tasteful properties of sugar have been domesticated as far back as 8000 BCE. With origins in New Guinea, the cultivation of sugar quickly spread over centuries of conquest and trade. The product, which quickly integrated into common foods and onto kitchen tables, is sucrose, which is made up of glucose and fructose dimers. While sugar is commonly associated with flavor, there is a myriad of biochemical properties that explain how sugars as biological molecules function in physiological contexts. Substantial research and reviews have been done on the role of glucose in disease. This review aims to describe the role of its isomers, fructose and mannose, in the context of inborn errors of metabolism and other metabolic diseases, such as cancer. While structurally similar, fructose and mannose give rise to very differing biochemical properties and understanding these differences will guide the development of more effective therapies for metabolic disease. We will discuss pathophysiology linked to perturbations in fructose and mannose metabolism, diagnostic tools, and treatment options of the diseases.

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“…The most important feature of EMT is downregulated E-cadherin (encoded by CDH1) expression. Some CDH1 transcriptional inhibitors, such as Snail, Slug, Twist, and ZEB1/2, have been identified (194)(195)(196).…”

Section: Metastasismentioning

confidence: 99%

Characterization of Histone Deacetylase Mechanisms in Cancer Development

Hai

Shu

et al. 2021

Front. Oncol.

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Over decades of studies, accumulating evidence has suggested that epigenetic dysregulation is a hallmark of tumours. Post-translational modifications of histones are involved in tumour pathogenesis and development mainly by influencing a broad range of physiological processes. Histone deacetylases (HDACs) and histone acetyltransferases (HATs) are pivotal epigenetic modulators that regulate dynamic processes in the acetylation of histones at lysine residues, thereby influencing transcription of oncogenes and tumour suppressor genes. Moreover, HDACs mediate the deacetylation process of many nonhistone proteins and thus orchestrate a host of pathological processes, such as tumour pathogenesis. In this review, we elucidate the functions of HDACs in cancer.

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Ketohexokinase-A acts as a nuclear protein kinase that mediates fructose-induced metastasis in breast cancer

Cited by 50 publications

References 44 publications

Fructose Metabolism in Cancer

Fructose Metabolism in Cancer

Fructose and Mannose in Inborn Errors of Metabolism and Cancer

Characterization of Histone Deacetylase Mechanisms in Cancer Development

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