4-Hydroxy-2-nonenal Induces Apoptosis by Inhibiting AKT Signaling in Human Osteosarcoma Cells

Ji, Guangrong; Yu, Naichun; Xue, Xiang; Li, Zong-guang

doi:10.1155/2014/873525

Cited by 26 publications

(19 citation statements)

References 30 publications

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“…Immunohistochemical staining of HNE adducts was demonstrated in animal models of liver cancer [110]. HNE treatment of MG63 human osteosarcoma cells could activate caspase-3 and altered the Bax/Bcl-2 ratio, thereby inducing cell death [111]. A recent research showed that HNE increased the growth of breast cancer cells and promoted their angiogenesis and invasion [112].…”

Section: Poducts Of Lipid Peroxidation As Common Markers Of Oxidativementioning

confidence: 99%

Mitochondrial dysfunction and oxidative stress in aging and cancer

et al. 2016

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Aging and cancer are the most important issues to research. The population in the world is growing older, and the incidence of cancer increases with age. There is no doubt about the linkage between aging and cancer. However, the molecular mechanisms underlying this association are still unknown. Several lines of evidence suggest that the oxidative stress as a cause and/or consequence of the mitochondrial dysfunction is one of the main drivers of these processes. Increasing ROS levels and products of the oxidative stress, which occur in aging and age-related disorders, were also found in cancer. This review focuses on the similarities between ageing-associated and cancer-associated oxidative stress and mitochondrial dysfunction as their common phenotype.

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Section: Poducts Of Lipid Peroxidation As Common Markers Of Oxidativementioning

confidence: 99%

Mitochondrial dysfunction and oxidative stress in aging and cancer

et al. 2016

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“…4-HNE may also interact with other proteins; for example, it forms adducts with His196, His267, Cys311, and Ser473 residues of AKT kinase, which results in a reduction in AKT sensitivity to phosphorylation. Additionally, modification of Ser473, considered to be the primary AKT regulatory site, leads to a decrease in the activity of the protein [56,57]. Because AKT has antiapoptotic effects through inhibiting several proapoptotic factors (including Acinus, AKS1, Bad, Bax, caspase-9) and activating antiapoptotic proteins (CREB and IKKα), suppression of AKT activity leads to a significant increase in apoptosis.…”

Section: Ros-dependent Lipid Peroxidation Productsmentioning

confidence: 99%

Involvement of Metabolic Lipid Mediators in the Regulation of Apoptosis

et al. 2020

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Apoptosis is the physiological mechanism of cell death and can be modulated by endogenous and exogenous factors, including stress and metabolic alterations. Reactive oxygen species (ROS), as well as ROS-dependent lipid peroxidation products (including isoprostanes and reactive aldehydes including 4-hydroxynonenal) are proapoptotic factors. These mediators can activate apoptosis via mitochondrial-, receptor-, or ER stress-dependent pathways. Phospholipid metabolism is also an essential regulator of apoptosis, producing the proapoptotic prostaglandins of the PGD and PGJ series, as well as the antiapoptotic prostaglandins of the PGE series, but also 12-HETE and 20-HETE. The effect of endocannabinoids and phytocannabinoids on apoptosis depends on cell type-specific differences. Cells where cannabinoid receptor type 1 (CB1) is the dominant cannabinoid receptor, as well as cells with high cyclooxygenase (COX) activity, undergo apoptosis after the administration of cannabinoids. In contrast, in cells where CB2 receptors dominate, and cells with low COX activity, cannabinoids act in a cytoprotective manner. Therefore, cell type-specific differences in the pro- and antiapoptotic effects of lipids and their (oxidative) products might reveal new options for differential bioanalysis between normal, functional, and degenerating or malignant cells, and better integrative biomedical treatments of major stress-associated diseases.

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“…HNE decreased AKT phosphorylation and activity in a wide concentration range from 5–100 μM in MG63 human osteosarcoma cells [77], 3T3-L1 adipocytes [78], human OA chondrocytes [79] and Jurkat cells [80]. In contrast, increased AKT phosphorylation was observed in vascular smooth muscle cells (1μM) [50], PC12 cells (15 μM) [81], human neuroblastoma IMR-32 cells (10 μM) [82], human corneal epithelial cells (30μM) [83] and retinal pigment epithelial (RPE) cells (0.1–5 μM) [84].…”

Section: Aging-related Signaling Pathways Affected By Hnementioning

confidence: 99%

4-hydroxynonenal-mediated signaling and aging

Zhang

2017

Free Radical Biology and Medicine

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4-Hydroxy-2-nonenal (HNE), one of the major α, β-unsaturated aldehydes produced during lipid peroxidation, is a potent messenger in mediating signaling pathways. Lipid peroxidation and HNE production appear to increase with aging. Although the cause and effect relation remains arguable, aging is associated with significant changes in diverse signaling events, characterized by enhanced or diminished responses of specific signaling pathways. In this review we will discuss how HNE may contribute to aging-related alterations of signaling pathways.

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4-Hydroxy-2-nonenal Induces Apoptosis by Inhibiting AKT Signaling in Human Osteosarcoma Cells

Cited by 26 publications

References 30 publications

Mitochondrial dysfunction and oxidative stress in aging and cancer

Mitochondrial dysfunction and oxidative stress in aging and cancer

Involvement of Metabolic Lipid Mediators in the Regulation of Apoptosis

4-hydroxynonenal-mediated signaling and aging

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