
Materials Today Bio, Journal Year: 2024, Volume and Issue: 29, P. 101317 - 101317
Published: Oct. 30, 2024
Language: Английский
Materials Today Bio, Journal Year: 2024, Volume and Issue: 29, P. 101317 - 101317
Published: Oct. 30, 2024
Language: Английский
Cancer Letters, Journal Year: 2023, Volume and Issue: 581, P. 216494 - 216494
Published: Nov. 24, 2023
Language: Английский
Citations
26Cancer Gene Therapy, Journal Year: 2024, Volume and Issue: 31(3), P. 349 - 363
Published: Jan. 4, 2024
Language: Английский
Citations
13Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15
Published: May 10, 2024
Cancer immunotherapy, such as immune checkpoint blockade (ICB), has emerged a groundbreaking approach for effective cancer treatment. Despite its considerable potential, clinical studies have indicated that the current response rate to immunotherapy is suboptimal, primarily attributed low immunogenicity in certain types of malignant tumors. Immunogenic cell death (ICD) represents form regulated (RCD) capable enhancing tumor and activating tumor-specific innate adaptive responses immunocompetent hosts. Therefore, gaining deeper understanding ICD evolution crucial developing more therapeutic strategies. This review focuses exclusively on both historical recent discoveries related modes their mechanistic insights, particularly within context immunotherapy. Our findings are also highlighted, revealing mode induction facilitated by atypical interferon (IFN)-stimulated genes (ISGs), including polo-like kinase 2 ( PLK2 ), during hyperactive type I IFN signaling. The concludes discussing potential ICD, with special attention relevance preclinical settings field
Language: Английский
Citations
13Advanced Science, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 20, 2025
Abstract Cuproptosis, a recently defined copper‐dependent cell death pathway, remains largely unexplored in tumor therapies, particularly breast cancer. This study demonstrates that triple‐negative cancer (TNBC) bears relatively elevated copper levels and exhibits resistance to cuproptosis. Mechanistically, activates the AKT signaling which inhibits ferredoxin‐1 (FDX1), key regulator of AKT1‐mediated FDX1 phosphorylation not only abrogates FDX1‐induced cuproptosis aerobic respiration but also promotes glycolysis. Consequently, combination AKT1 inhibitors ionophores synergistically alleviate TNBC tumorigenesis both vitro vivo. In summary, findings reveal crucial mechanism underlying suggest potential therapeutic approach for TNBC.
Language: Английский
Citations
1Trends in cancer, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 1, 2025
Language: Английский
Citations
1Cancer Letters, Journal Year: 2023, Volume and Issue: 571, P. 216348 - 216348
Published: Aug. 9, 2023
Language: Английский
Citations
20Frontiers in Oncology, Journal Year: 2023, Volume and Issue: 13
Published: Nov. 7, 2023
The sustenance of human life activities depends on copper, which also serves as a crucial factor for vital enzymes. Under typical circumstances, active homeostatic mechanisms keep the intracellular copper ion concentration low. Excess ions cause excessive cellular respiration, causes cytotoxicity and cell death levels steadily rise above threshold. It is novel that mitochondrial ions, regulation. Cuproptosis now understood to play role in several pathogenic processes, including inflammation, oxidative stress, apoptosis. Copper type regulatory death(RCD).Numerous diseases are correlated with development homeostasis imbalances. One most popular areas study field cancer cuproptosis. has been discovered angiogenesis, proliferation, growth, metastasis all accumulation ions. concentrations can serve marker development. In order reference clinical research product, diagnosis, treatment cancer, this paper covers function imbalance malignant cancers related molecular pathways.
Language: Английский
Citations
19Antioxidants and Redox Signaling, Journal Year: 2023, Volume and Issue: unknown
Published: Feb. 2, 2023
Significance: As a redox-sensitive protein, high-mobility group box 1 (HMGB1) is implicated in regulating stress responses to oxidative damage and cell death, which are closely related the pathology of inflammatory diseases, including cancer. Recent advances: HMGB1 non-histone nuclear protein that acts as DNA chaperone control chromosomal structure function. can also be released into extracellular space function damage-associated molecular pattern during apoptosis, necrosis, necroptosis, pyroptosis, ferroptosis, alkaliptosis, cuproptosis. Once released, binds membrane receptors shape immune metabolic responses. In addition subcellular localization, activity depends on its redox state posttranslational modifications. Abnormal plays dual role tumorigenesis anticancer therapy (e.g., chemotherapy, radiation therapy, immunotherapy) depending tumor types stages. Critical issues: A comprehensive understanding cellular homeostasis important for deciphering normal functions pathological manifestations. this review, we discuss compartmental-defined roles death Understanding these advances may help us develop potential HMGB1-targeting drugs or approaches treat stress-related diseases conditions. Future directions: Further studies required dissect mechanism by maintains under different multidisciplinary effort evaluate applications precisely targeting pathway human health disease.
Language: Английский
Citations
17Frontiers in Aging Neuroscience, Journal Year: 2024, Volume and Issue: 16
Published: April 23, 2024
The expanding geriatric population, whose predisposition toward disabling morbidities and age-related diseases (ARD) is well-documented, has become a paramount social issue, exerting an onerous burden on both the healthcare industry wider society. ARD manifest as progressive deterioration of bodily tissues organs, eventually resulting in failure these vital components. At present, no efficacious measures exist to hinder onset ARD. Copper, essential trace element, involved wide range physiological processes across different cell types. In recent research, novel variant copper-dependent death, termed cuproptosis, been identified. This mode cellular demise stands apart from previously recognized types death. Cuproptosis occurs when copper binds with acyl-CoA synthetase tricarboxylic acid (TCA) cycle, protein aggregation toxicity stress, ultimately leading this paper, we provide concise overview current understanding concerning metabolism copper, copper-related diseases, hallmarks toxicity, mechanisms that regulate toxicity. Additionally, discuss implications cuproptosis mutations development ARD, well potential for targeting treatment
Language: Английский
Citations
8Seminars in Cancer Biology, Journal Year: 2024, Volume and Issue: 106-107, P. 123 - 142
Published: Sept. 30, 2024
Language: Английский
Citations
7