Phytomedicine, Journal Year: 2024, Volume and Issue: 136, P. 156303 - 156303
Published: Dec. 4, 2024
Abnormal antioxidant capacity in cancer cells is intimately linked to tumor aggressiveness. Modulating oxidative stress status and inhibiting ferroptosis represents a novel anticancer therapeutic strategy. STAM Binding Protein Like 1 (STAMBPL1), deubiquitinase, implicated various malignancies, yet its function potential for cholangiocarcinoma (CCA) remains unexplored.
Language: Английский
Molecular Cancer, Journal Year: 2024, Volume and Issue: 23(1)
Published: Sept. 6, 2024
Language: Английский
Citations
42
Redox Biology, Journal Year: 2024, Volume and Issue: 75, P. 103259 - 103259
Published: June 27, 2024
Ferroptosis is a form of iron-related oxidative cell death governed by an integrated redox system, encompassing pro-oxidative proteins and antioxidative proteins. These undergo precise control through diverse post-translational modifications, including ubiquitination, phosphorylation, acetylation, O-GlcNAcylation, SUMOylation, methylation, N-myristoylation, palmitoylation, modification. modifications play pivotal roles in regulating protein stability, activity, localization, interactions, ultimately influencing both the buildup iron lipid peroxidation. In mammalian cells, regulators ferroptosis typically degradation via two principal pathways: ubiquitin-proteasome which handles majority degradation, autophagy, primarily targeting long-lived or aggregated This comprehensive review aims to summarize recent advances modification linked ferroptosis. It also discusses strategies for modulating systems, providing new insights into potential therapeutic applications cancer non-neoplastic diseases.
Language: Английский
Citations
16
Antioxidants, Journal Year: 2024, Volume and Issue: 13(6), P. 697 - 697
Published: June 6, 2024
Glutathione (GSH), a prominent antioxidant in organisms, exhibits diverse biological functions and is crucial safeguarding cells against oxidative harm upholding stable redox milieu. The metabolism of GSH implicated numerous diseases, particularly the progression malignant tumors. Consequently, therapeutic strategies targeting regulation synthesis to modulate levels represent promising avenue for future research. This study aimed elucidate intricate relationship between ferroptosis, highlighting how modulation can impact cellular susceptibility ferroptosis consequently influence development tumors other diseases. paper provides comprehensive overview physiological GSH, including its structural characteristics, physicochemical properties, sources, metabolic pathways, as well investigate molecular mechanisms underlying potential interventions. Unraveling role holds promise individuals afflicted with
Language: Английский
Citations
14
European Journal of Pharmacology, Journal Year: 2024, Volume and Issue: 972, P. 176553 - 176553
Published: April 2, 2024
Stroke poses a significant risk of mortality, particularly among the elderly population. The pathophysiological process ischemic stroke is complex, and it crucial to elucidate its molecular mechanisms explore potential protective drugs. Ferroptosis, newly recognized form programmed cell death distinct from necrosis, apoptosis, autophagy, closely associated with pathophysiology stroke. N6022, selective inhibitor S-nitrosoglutathione reductase (GSNOR), "first-in-class" drug for asthma therapeutic applications. However, remains unclear whether N6022 exerts effects in stroke, precise action are unknown. This study aimed investigate mitigates cerebral ischemia/reperfusion (I/R) injury by reducing ferroptosis underlying mechanisms. Accordingly, we established an oxygen-glucose deprivation/reperfusion (OGD/R) model middle artery occlusion/reperfusion (MCAO/R) mouse mimic I/R injury. Our data, both vitro vivo, demonstrated that effectively protected against I/R-induced brain damage neurological deficits mice, as well OGD/R-induced BV2 damage. Mechanistically, promoted Nrf2 nuclear translocation, enhancing intracellular antioxidant capacity SLC7A11-GPX4 system. Furthermore, interfered interaction GSNOR GSTP1, thereby boosting GSTP1 attenuating ferroptosis. These findings provide novel insights, showing attenuates microglial induced through promotion translocation inhibition GSNOR/GSTP1 axis.
Language: Английский
Citations
9
Life Sciences, Journal Year: 2025, Volume and Issue: unknown, P. 123565 - 123565
Published: March 1, 2025
Language: Английский
Citations
1
International Journal of Biological Macromolecules, Journal Year: 2024, Volume and Issue: 276, P. 133792 - 133792
Published: July 9, 2024
Language: Английский
Citations
8
Phytomedicine, Journal Year: 2024, Volume and Issue: 134, P. 155989 - 155989
Published: Aug. 31, 2024
Language: Английский
Citations
8
Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15
Published: Sept. 30, 2024
Cancer, the world’s second leading cause of death after cardiovascular diseases, is characterized by hallmarks such as uncontrolled cell growth, metastasis, angiogenesis, hypoxia, and resistance to therapy. Autophagy, a cellular process that can both support inhibit cancer progression, plays critical role in development progression. This involves formation autophagosomes ultimately fuse with lysosomes degrade components. A key regulator this Sirtuin 1 (SIRT1), which significantly influences autophagy. review delves into SIRT1 modulating autophagy its broader impacts on carcinogenesis. regulates crucial mediators, AMP-activated protein kinase (AMPK) mammalian target rapamycin (mTOR), effectively promoting or suppressing Beyond direct effects autophagy, SIRT1’s regulatory actions extend other processes, including apoptosis ferroptosis, thereby influencing tumor proliferation, chemotherapy responses. These insights underscore complex interplay between significant implications for Targeting associated pathways presents promising strategy manipulate treatment. underscores potential therapeutic target, opening new avenues enhancing treatment efficacy.
Language: Английский
Citations
5
Pharmacological Research, Journal Year: 2024, Volume and Issue: 210, P. 107490 - 107490
Published: Nov. 5, 2024
The emergence of sorafenib resistance has become a predominant impediment and formidable dilemma in the therapeutic approach for hepatocellular carcinoma (HCC). Although approval next-generation drugs as alternatives to is significant development, concurrent use inhibitors that target additional key molecular pathways remains an effective strategy mitigate acquisition resistance. Here, we identified Glutathione S-Transferase Alpha 1 (GSTA1) critical modulator (SR) (HCC) based on our findings from experiments conducted recurrent liver cancer tissues, xenograft mouse models, organoids, sorafenib-resistant cells. Elevated GSTA1 levels are strongly associated with adverse clinical prognoses. knockout reinstates sensitivity, whereas its overexpression attenuates drug efficacy. Mechanistically, enhances accumulation lipid peroxides suppresses ferroptosis by exerting peroxidase function regulate SR. Notably, upregulation expression mediated transcription factor CTNNB1 (β-catenin), resulting formation cytoplasmic complex between CTNNB1. This facilitates nuclear translocation CTNNB1, establishing positive feedback loop. combined demonstrated synergistic anti-tumour effects through induction both vitro vivo. Our reveal novel regulatory role GSTA1/CTNNB1 axis ferroptosis, suggesting targeting could be promising circumvent HCC.
Language: Английский
Citations
4
Antioxidants, Journal Year: 2025, Volume and Issue: 14(2), P. 189 - 189
Published: Feb. 6, 2025
Current research suggests that promoting ferroptosis, a non-apoptotic form of cell death, may be an effective therapy for osteosarcoma, while its inhibition could facilitate bone regeneration and prevent osteoporosis. Our objective was to investigate whether the susceptibility regulation ferroptosis differ between undifferentiated (UBC) differentiated (DBC) human marrow stromal cells, as well osteosarcoma cells (MG63). Ferroptosis induced by either inhibiting glutathione peroxidase 4 (GPX4) using RSL3 or blocking all glutathione-dependent enzymes through glutamate/cysteine antiporter with Erastin. Lipid peroxidation assessed fluorescent probe BODIPY™581/591C11, Ferrostatin-1 used inhibit ferroptosis. We demonstrate neither Erastin nor induces in DBC. However, both induce UBC, predominantly MG63 cells. data suggest induction hBMSCs is primarily regulated GPX4, whereas S-Transferase P1 (GSTP1) plays key role controlling In conclusion, targeting pathways involved across different types improve efficacy cancer treatments minimizing collateral damage supporting regenerative processes, minimal impact on therapy.
Language: Английский
Citations
0