The Redox Role of G6PD in Cell Growth, Cell Death, and Cancer

Cells, Год журнала: 2019, Номер 8(9), С. 1055 - 1055

Опубликована: Сен. 8, 2019

The generation of reducing equivalent NADPH via glucose-6-phosphate dehydrogenase (G6PD) is critical for the maintenance redox homeostasis and reductive biosynthesis in cells. also plays key roles cellular processes mediated by signaling. Insufficient G6PD activity predisposes cells to growth retardation demise. Severely lacking impairs embryonic development delays organismal growth. Altered associated with pathophysiology, such as autophagy, insulin resistance, infection, inflammation, well diabetes hypertension. Aberrant activation leads enhanced cell proliferation adaptation many types cancers. present review aims update existing knowledge concerning emphasizes how modulates signaling affects survival demise, particularly diseases cancer. Exploiting a potential drug target against cancer discussed.

Язык: Английский

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Targeting ferroptosis in breast cancer

Biomarker Research, Год журнала: 2020, Номер 8(1)

Опубликована: Ноя. 5, 2020

Abstract Ferroptosis is a recently discovered distinct type of regulated cell death caused by the accumulation lipid-based ROS. Metabolism and expression specific genes affect occurrence ferroptosis, making it promising therapeutic target to manage cancer. Here, we describe current status ferroptosis studies in breast cancer trace key regulators back previous studies. We also compare common patterns discuss sensitivity different subtypes propose that viewing ferroptosis-related from historical angle will accelerate development ferroptosis-based biomarkers strategies

Язык: Английский

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TIGAR drives colorectal cancer ferroptosis resistance through ROS/AMPK/SCD1 pathway

Free Radical Biology and Medicine, Год журнала: 2022, Номер 182, С. 219 - 231

Опубликована: Март 1, 2022

Язык: Английский

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Hypoxia, oxidative stress, and the interplay of HIFs and NRF2 signaling in cancer

Experimental & Molecular Medicine, Год журнала: 2024, Номер 56(3), С. 501 - 514

Опубликована: Март 1, 2024

Abstract Oxygen is crucial for life and acts as the final electron acceptor in mitochondrial energy production. Cells adapt to varying oxygen levels through intricate response systems. Hypoxia-inducible factors (HIFs), including HIF-1α HIF-2α, orchestrate cellular hypoxic response, activating genes increase supply reduce expenditure. Under conditions of excess resulting oxidative stress, nuclear factor erythroid 2-related 2 (NRF2) activates hundreds oxidant removal adaptive cell survival. Hypoxia stress are core hallmarks solid tumors activated HIFs NRF2 play pivotal roles tumor growth progression. The complex interplay between hypoxia within microenvironment adds another layer intricacy HIF signaling This review aimed elucidate dynamic changes functions pathways emphasizing their implications milieu. Additionally, this explored elaborate NRF2, providing insights into significance these interactions development novel cancer treatment strategies.

Язык: Английский

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Emerging role of NRF2 in ROS-mediated tumor chemoresistance

Biomedicine & Pharmacotherapy, Год журнала: 2020, Номер 131, С. 110676 - 110676

Опубликована: Авг. 25, 2020

Chemoresistance is a central cause for the tumor management failure. Cancer cells disrupt redox homeostasis through reactive oxygen species (ROS) regulatory mechanisms, leading to progression and chemoresistance. The transcription factor nuclear erythroid 2-related 2 (NRF2) master regulator of neutralizing cellular ROS restoring balance. Understanding role NRF2 in ROS-mediated chemoresistance can be helpful development chemotherapy strategies with better efficiency. In this review, we sum up roles classical agents including cisplatin, 5-fluorouracil, gemcitabine, oxaliplatin, paclitaxel, doxorubicin, how overcome by targeting NRF2. Finally, propose that might promising strategy resist ROS-driven acquire efficacy cancer treatment.

Язык: Английский

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Potential Applications of NRF2 Modulators in Cancer Therapy

Antioxidants, Год журнала: 2020, Номер 9(3), С. 193 - 193

Опубликована: Фев. 25, 2020

The nuclear factor erythroid 2-related 2 (NRF2)-Kelch-like ECH-associated protein 1 (KEAP1) regulatory pathway plays an essential role in protecting cells and tissues from oxidative, electrophilic, xenobiotic stress. By controlling the transactivation of over 500 cytoprotective genes, NRF2 transcription has been implicated physiopathology several human diseases, including cancer. In this respect, accumulating evidence indicates that can act as a double-edged sword, being able to mediate tumor suppressive or pro-oncogenic functions, depending on specific biological context its activation. Thus, better understanding mechanisms control functions most appropriate activation is prerequisite for development effective therapeutic strategies based modulation. line principle, controlled might reduce risk cancer initiation normal by scavenging reactive-oxygen species (ROS) preventing genomic instability through decreased DNA damage. contrast however, already transformed with constitutive prolonged signaling represent major clinical hurdle exhibit aggressive phenotype characterized therapy resistance unfavorable prognosis, requiring use inhibitors. review, we will focus dual roles NRF2-KEAP1 promotion inhibition, describing potential context-specific modulation NRF2.

Язык: Английский

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Emerging role of ferroptosis in breast cancer: New dawn for overcoming tumor progression

Pharmacology & Therapeutics, Год журнала: 2021, Номер 232, С. 107992 - 107992

Опубликована: Окт. 1, 2021

Язык: Английский

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Nuclear Factor Erythroid 2-Related Factor 2 in Regulating Cancer Metabolism

Antioxidants and Redox Signaling, Год журнала: 2020, Номер 33(13), С. 966 - 997

Опубликована: Янв. 28, 2020

Significance: Nuclear factor erythroid 2 (NFE2)-related (NFE2L2, or NRF2) is a transcription predominantly affecting the expression of antioxidant genes. NRF2 plays significant role in control redox balance, which crucial cancer cells. activation regulates numerous hallmarks, including metabolism, stem cell characteristics, tumor aggressiveness, invasion, and metastasis formation. We review molecular characteristics pathway discuss its interactions with hallmarks previously listed. Recent Advances: The noncanonical was recently discovered, members this are involved carcinogenesis. Further, cancer-related changes (e.g., metabolic flexibility) that support progression were found to be redox- dependent. Critical Issues: undergoes Janus-faced behavior cancers. pro- antineoplastic effects context dependent essentially based on specific question. Therefore, systematic investigation signaling necessary clarify etiology. biggest challenge field determine cancers can targeted for better clinical outcomes. large-scale genomic transcriptomic studies missing correlate outcome activity system. Future Directions: To exploit setting future, druggable should identified. In addition, it will important study how modulation system interferes cytostatic drugs their combinations.

Язык: Английский

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Nrf2 Modulation in Breast Cancer

Biomedicines, Год журнала: 2022, Номер 10(10), С. 2668 - 2668

Опубликована: Окт. 21, 2022

Reactive oxygen species (ROS) are identified to control the expression and activity of various essential signaling intermediates involved in cellular proliferation, apoptosis, differentiation. Indeed, ROS represents a double-edged sword supporting cell survival death. Many common pathological processes, including cancer types neurodegenerative diseases, inflammation oxidative stress triggers, or even initiate them. Keap1-Nrf2 is master antioxidant pathway cytoprotective mechanisms through Nrf2 target gene expression. Activation Nfr2 benefits cells early stages reduces level ROS. In contrast, hyperactivation creates context that supports both healthy cancerous cells, defending them against stress, chemotherapeutic drugs, radiotherapy. Considering dual role suppressing expanding determining its inhibitory/stimulatory position targeting can represent an impressive treatment. This review focused on modulators their roles sensitizing breast chemo/radiotherapy agents.

Язык: Английский

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LINC00242/miR-1-3p/G6PD axis regulates Warburg effect and affects gastric cancer proliferation and apoptosis

Molecular Medicine, Год журнала: 2021, Номер 27(1)

Опубликована: Янв. 29, 2021

Reprogrammed glucose metabolism of enhanced Warburg effect (or aerobic glycolysis) is considered as a hallmark cancer. Long non-coding RNAs (lncRNAs) have been certified to play crucial role in tumor progression. The current study aims inquire into the potential regulatory mechanism long intergenic non-protein coding RNA 242 (LINC00242) on glycolysis gastric cancer.LINC00242, miR-1-3p and G6PD expression levels cancer tissues cells were determined by qRT-PCR. Cell apoptosis or viability examined Flow cytometry MTT assay. Western blot was utilized investigate protein levels. Immunohistochemical (IHC) hematoxylin eosin (H&E) staining used for histopathological detection. targeted relationship between LINC00242 verified luciferase reporter gene Nude mouse xenograft detect formation vivo.LINC00242 high-expressed cells, positively correlated with G6PD. Silencing within prominently inhibited cell proliferation vitro relieved tumorigenesis vivo. predicted directly target both Overexpression suppressed glycolysis. competitively combined miR-1-3p, therefore relieving miR-1-3p-mediated suppression G6PD.LINC00242 plays stimulative via regulation miR-1-3p/ axis, affecting proliferation.

Язык: Английский

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