Relationship between Glutathione-Dependent Enzymes and the Immunohistochemical Profile of Glial Neoplasms

Обухова, Л. М.; Копытова, Т. В.; Murach, Elena; Щелчкова, Н А; Kontorshchikova, Claudia; Medyanik, Igor; Orlinskaya, N.Yu.; Grishin, Artem; Kontorshchikov, Michael; Badanina, Dariya

doi:10.3390/biomedicines10102393

Cited by 3 publications

(1 citation statement)

References 47 publications

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“…Brain tissues in the peritumoral area show evidence of oxidative stress, manifested through increased production of reactive oxygen species (ROS) and decreased antioxidant-enzyme defenses such as catalase, glutathione peroxidase, and superoxide dismutase (17,18). The oxidative stress in the glioma microenvironment is closely related to iron homeostasis, since the balanced amount of intracellular iron governs the oxidation state of phospolipids (19,20) (Figure 1).…”

Section: Introductionmentioning

confidence: 99%

Ferroptosis and PPAR-gamma in the limelight of brain tumors and edema

Yakubov,

Schmid,

Hammer

et al. 2023

Front. Oncol.

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Human malignant brain tumors such as gliomas are devastating due to the induction of cerebral edema and neurodegeneration. A major contributor to glioma-induced neurodegeneration has been identified as glutamate. Glutamate promotes cell growth and proliferation in variety of tumor types. Intriguently, glutamate is also an excitatory neurotransmitter and evokes neuronal cell death at high concentrations. Even though glutamate signaling at the receptor and its downstream effectors has been extensively investigated at the molecular level, there has been little insight into how glutamate enters the tumor microenvironment and impacts on metabolic equilibration until recently. Surprisingly, the 12 transmembrane spanning tranporter xCT (SLC7A11) appeared to be a major player in this process, mediating glutamate secretion and ferroptosis. Also, PPARγ is associated with ferroptosis in neurodegeneration, thereby destroying neurons and causing brain swelling. Although these data are intriguing, tumor-associated edema has so far been quoted as of vasogenic origin. Hence, glutamate and PPARγ biology in the process of glioma-induced brain swelling is conceptually challenging. By inhibiting xCT transporter or AMPA receptors in vivo, brain swelling and peritumoral alterations can be mitigated. This review sheds light on the role of glutamate in brain tumors presenting the conceptual challenge that xCT disruption causes ferroptosis activation in malignant brain tumors. Thus, interfering with glutamate takes center stage in forming the basis of a metabolic equilibration approach.

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Section: Introductionmentioning

confidence: 99%

Ferroptosis and PPAR-gamma in the limelight of brain tumors and edema

Yakubov,

Schmid,

Hammer

et al. 2023

Front. Oncol.

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Evaluation of In Vitro Biological Activity of Flavanone/Chromanone Derivatives: Molecular Analysis of Anticancer Mechanisms in Colorectal Cancer

Hikisz,

Wawrzyniak,

Adamus-Grabicka

et al. 2024

IJMS

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The primary objective of this study was to evaluate the anticancer activity of six flavanone/chromanone derivatives: 3-benzylideneflavanones/3-benzylidenechroman-4-ones and their 3-spiro-1-pirazolines analogs. We employed five colon cancer cell lines with varying degrees of metastasis and genetic profiles as our research model. Our investigation focused primarily on assessing the pro-oxidant properties of the tested derivatives and their impact on overall antiproliferative activity. To comprehensively evaluate the cytotoxic properties of these compounds, we analyzed their genotoxic, pro-apoptotic, and autophagy-inducing effects. Our findings indicate that three of the six analyzed derivatives exhibited promising antiproliferative activity against cancer cells, with IC50 values ranging from 10 to 30 μM. Strong pro-oxidant properties were identified as a key mechanism underlying their cytotoxic activity. The generation of oxidative stress, which varied depending on the specific flavanone/chromanone derivative, resulted from increased intracellular reactive oxygen species (ROS) levels and decreased glutathione (GSH) concentrations. Furthermore, oxidative stress likely contributed to the induction of apoptosis/autophagy in cancer cells and the emergence of significant DNA damage.

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Epigenetic Mechanisms of Endocrine-Disrupting Chemicals in Breast Cancer and Their Impact on Dietary Intake

Singh

2024

JoX

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Addressing the consequences of exposure to endocrine-disrupting chemicals (EDCs) demands thorough research and elucidation of the mechanism by which EDCs negatively impact women and lead to breast cancer (BC). Endocrine disruptors can affect major pathways through various means, including histone modifications, the erroneous expression of microRNA (miRNA), DNA methylation, and epigenetic modifications. However, it is still uncertain if the epigenetic modifications triggered by EDCs can help predict negative outcomes. Consequently, it is important to understand how different endocrine disrupters or signals interact with epigenetic modifications and regulate signalling mechanisms. This study proposes that the epigenome may be negatively impacted by several EDCs, such as cadmium, arsenic, lead, bisphenol A, phthalates, polychlorinated biphenyls and parabens, organochlorine, and dioxins. Further, this study also examines the impact of EDCs on lifestyle variables. In breast cancer research, it is essential to consider the potential impacts of EDC exposure and comprehend how EDCs function in tissues.

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Relationship between Glutathione-Dependent Enzymes and the Immunohistochemical Profile of Glial Neoplasms

Cited by 3 publications

References 47 publications

Ferroptosis and PPAR-gamma in the limelight of brain tumors and edema

Ferroptosis and PPAR-gamma in the limelight of brain tumors and edema

Evaluation of In Vitro Biological Activity of Flavanone/Chromanone Derivatives: Molecular Analysis of Anticancer Mechanisms in Colorectal Cancer

Epigenetic Mechanisms of Endocrine-Disrupting Chemicals in Breast Cancer and Their Impact on Dietary Intake

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