Hybrid Compounds &amp; Oxidative Stress Induced Apoptosis in Cancer Therapy

Hanikoğlu, Aysegul; Özben, Hakan; Hanikoglu, Ferhat; Özben, Tomris

doi:10.2174/0929867325666180719145819

Cited by 36 publications

(24 citation statements)

References 107 publications

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“…Therefore, science faces the need to determine the cases-depending on the type of cells involved-in which therapeutic strategy should be used. This could represent proapoptotic effects, in the case of cancer [155,156], or antiapoptotic effects, for example, in the protection against neurodegenerative disorders [157]. Given the possibility of the modification of cell phospholipid metabolisms by exogenous compounds, there are real possibilities of modulating the cell death process, depending on the needs of therapy.…”

Section: Discussionmentioning

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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Section: Discussionmentioning

confidence: 99%

Involvement of Metabolic Lipid Mediators in the Regulation of Apoptosis

et al. 2020

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“…Moreover, the oxidative stress would be aggravated by the continuous generated ROS stimulated by exogenous and endogenous factors, which will induce apoptosis and necrosis once the ROS levels exceed the tolerance of tumor cells. However, due to the relatively lower ROS basic level, such situation usually does not appear in normal cells 10–12. Therefore, regulating intracellular ROS signal to selectively kill tumor cells without affecting normal cells can be an effective strategy for tumor therapy 13.…”

Section: Introductionmentioning

confidence: 99%

<p>Regulating intracellular ROS signal by a dual pH/reducing-responsive nanogels system promotes tumor cell apoptosis</p>

Dong¹,

Lei²,

Guo³

et al. 2019

IJN

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Purpose: The levels of reactive oxygen species (ROS) in tumor cells are much higher than that in normal cells, and rise rapidly under the influence of exogenous or endogenous inducing factors, eventually leading to the apoptosis of tumor cells. Therefore, this study prepared a dual pH/reducing-responsive poly ( N -isopropylacrylamide-co-Cinnamaldehyde-co-D-α-tocopheryl polyethylene glycol 1000 succinate, P ss NCT) nanogels, which employed two exogenous ROS inducers, cinnamaldehyde (CA) and D-α-tocopheryl polyethylene glycol 1000 succinate (TPGS), to selectively induce apoptosis by regulating ROS levels in tumor cells. Methods: The P ss NCT nanogels were prepared by the free radical precipitation polymerization under the crosslink between pH-sensitive hydrazone and reducing-sensitive disulfide bonds, followed by the physicochemical and morphological characteristics investigations. Plasma stability, dual pH/reducing responsive degradation and in vitro release were also assessed. In cell experiments, cytotoxicity in different cells were first detected. The intracellular ROS levels and mitochondrial functions of tumor cells were then evaluated. Moreover, the apoptosis and western-blot assays were employed to verify the association between ROS levels elevation and apoptosis in tumor cells. Results: The nanogels exhibited a round-like hollow structure with the diameter smaller than 200nm. The nanogels were stable in plasma, while showed rapid degradation in acidic and reducing environments, thus achieving significant release of CA and TPGS in these media. Furthermore, the sufficient amplification of ROS signals was induced by the synergistically function of CA and TPGS on mitochondria, which resulted in the opening of the mitochondrial apoptotic pathway and enhanced cytotoxicity on MCF-7 cells. However, nanogels barely affected L929 cells owing to their lower intracellular ROS basal levels. Conclusion: The specific ROS regulation method achieved by these nanogels could be explored to selectively kill tumor cells according to the difference of ROS signals in different kinds of cells.

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“…It has been demonstrated that miRNA-346 is induced under ER stress, and it is involved in autophagy/mitophagy activation to facilitate cell survival [191]. In fact, an increase of ROS during ER stress can be harmful to cancer cells [192]. In this scenario, miRNA-346 promoted mitophagy activation via GSK3 β and reduced ROS preserving cell viability [191].…”

Section: Mitophagy and Rosmentioning

confidence: 99%

Mitophagy and Oxidative Stress in Cancer and Aging: Focus on Sirtuins and Nanomaterials

Vernucci

Tomino

Molinari

et al. 2019

Oxidative Medicine and Cellular Longevity

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Mitochondria are the cellular center of energy production and of several important metabolic processes. Mitochondrion health is maintained with a substantial intervention of mitophagy, a process of macroautophagy that degrades selectively dysfunctional and irreversibly damaged organelles. Because of its crucial duty, alteration in mitophagy can cause functional and structural adjustment in the mitochondria, changes in energy production, loss of cellular adaptation, and cell death. In this review, we discuss the dual role that mitophagy plays in cancer and age-related pathologies, as a consequence of oxidative stress, evidencing the triggering stimuli and mechanisms and suggesting the molecular targets for its therapeutic control. Finally, a section has been dedicated to the interplay between mitophagy and therapies using nanoparticles that are the new frontier for a direct and less invasive strategy.

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Hybrid Compounds & Oxidative Stress Induced Apoptosis in Cancer Therapy

Cited by 36 publications

References 107 publications

Involvement of Metabolic Lipid Mediators in the Regulation of Apoptosis

Involvement of Metabolic Lipid Mediators in the Regulation of Apoptosis

<p>Regulating intracellular ROS signal by a dual pH/reducing-responsive nanogels system promotes tumor cell apoptosis</p>

Mitophagy and Oxidative Stress in Cancer and Aging: Focus on Sirtuins and Nanomaterials

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