The role of the TNF receptors and apoptosis inducing ligands in tumor growth

Minchenko, О. H.; Tsymbal, Dariia O.; Minchenko, Dmytro O.; Ratushna, O O

doi:10.15407/ubj88.05.018

Cited by 10 publications

(5 citation statements)

References 92 publications

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“…The extrinsic apoptotic pathway is driven by the ligand-receptor interaction between death-inducing ligands such as Fas ligand (FasL) and tumor necrosis factor (TNF) and their respective receptors Fas receptor (FasR) and TNF receptor (TNFR) 140 , 141 . After the ligand-receptor interaction, an adaptor protein (FADD for FasR and TRADD for TNFR), receptor-interacting protein kinase 1 (RIP1) and procaspase-8 are recruited to form the death-inducing signaling complex (DISC) and subsequently induce apoptosis 142 .…”

Section: Ros a Double-edged Sword In Cancer Progressionmentioning

confidence: 99%

The double-edged roles of ROS in cancer prevention and therapy

et al. 2021

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Reactive oxygen species (ROS) serve as cell signaling molecules generated in oxidative metabolism and are associated with a number of human diseases. The reprogramming of redox metabolism induces abnormal accumulation of ROS in cancer cells. It has been widely accepted that ROS play opposite roles in tumor growth, metastasis and apoptosis according to their different distributions, concentrations and durations in specific subcellular structures. These double-edged roles in cancer progression include the ROS-dependent malignant transformation and the oxidative stress-induced cell death. In this review, we summarize the notable literatures on ROS generation and scavenging, and discuss the related signal transduction networks and corresponding anticancer therapies. There is no doubt that an improved understanding of the sophisticated mechanism of redox biology is imperative to conquer cancer.

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Section: Ros a Double-edged Sword In Cancer Progressionmentioning

confidence: 99%

The double-edged roles of ROS in cancer prevention and therapy

et al. 2021

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“…TNF-α is a pro-inflammatory cytokine with diverse roles, e.g., it can favor tumor development, angiogenesis, as well as apoptosis and recruitment of macrophages (resident of the CNS or infiltrates). The variety of effects of TNF-α results from its ability to interact with a number of receptors, leading to the activation of several intracellular pathways [202]. Some authors address the role of flavonoids as naringin, apigenin, fisentin and quercetin in the regulation of IL-1β in the tumoral context [203,204].…”

Section: Neuroimmunomodulatory Action Of Flavonoids and Derivativesmentioning

confidence: 99%

Neuroimmunomodulatory Properties of Flavonoids and Derivates: A Potential Action as Adjuvants for the Treatment of Glioblastoma

et al. 2022

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Glioblastomas (GBMs) are tumors that have a high ability to migrate, invade and proliferate in the healthy tissue, what greatly impairs their treatment. These characteristics are associated with the complex microenvironment, formed by the perivascular niche, which is also composed of several stromal cells including astrocytes, microglia, fibroblasts, pericytes and endothelial cells, supporting tumor progression. Further microglia and macrophages associated with GBMs infiltrate the tumor. These innate immune cells are meant to participate in tumor surveillance and eradication, but they become compromised by GBM cells and exploited in the process. In this review we discuss the context of the GBM microenvironment together with the actions of flavonoids, which have attracted scientific attention due to their pharmacological properties as possible anti-tumor agents. Flavonoids act on a variety of signaling pathways, counteracting the invasion process. Luteolin and rutin inhibit NFκB activation, reducing IL-6 production. Fisetin promotes tumor apoptosis, while inhibiting ADAM expression, reducing invasion. Naringenin reduces tumor invasion by down-regulating metalloproteinases expression. Apigenin and rutin induce apoptosis in C6 cells increasing TNFα, while decreasing IL-10 production, denoting a shift from the immunosuppressive Th2 to the Th1 profile. Overall, flavonoids should be further exploited for glioma therapy.

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“…Such involvement of free-radical reactions, aroused in membranes of the endoplasmic reticulum in response to stress, has been recently reported in a number of recent works [38].…”

Section: The General Toxic Effects Of Cadmium Compoundsmentioning

confidence: 73%

Biochemical mechanisms of free-radical damage to the nuclear genome by cadmium

Trakhtenberg¹,

Gubsky²,

Levitsky³

et al. 2018

Ukr.Biochem.J

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has been used for many years in industry and agriculture. Its active use is associated with a danger to human health due to a significant toxic effect on the body. The purpose of the review was to analyze the literature data and the results of our own experimental research on the biochemical mechanisms of the toxic effect of cadmium on the nuclear chromatin of cells, primarily the liver. Based on this analysis, the concept that the toxicity of cadmium is associated with damage caused by cadmium-induced free radicals was confirmed. The reactive oxygen species formed in this way are active damaging agents that cause toxic effects, including mutagenic, which ultimately leads to apoptosis and cell death.

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The role of the TNF receptors and apoptosis inducing ligands in tumor growth

Cited by 10 publications

References 92 publications

The double-edged roles of ROS in cancer prevention and therapy

The double-edged roles of ROS in cancer prevention and therapy

Neuroimmunomodulatory Properties of Flavonoids and Derivates: A Potential Action as Adjuvants for the Treatment of Glioblastoma

Biochemical mechanisms of free-radical damage to the nuclear genome by cadmium

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