The Science of The Total Environment, Год журнала: 2024, Номер 954, С. 176353 - 176353
Опубликована: Сен. 19, 2024
Immunological Reviews, Год журнала: 2023, Номер 321(1), С. 211 - 227
Опубликована: Сен. 16, 2023
Summary Copper is an essential nutrient for maintaining enzyme activity and transcription factor function. Excess copper results in the aggregation of lipoylated dihydrolipoamide S‐acetyltransferase (DLAT), which correlates to mitochondrial tricarboxylic acid (TCA) cycle, resulting proteotoxic stress eliciting a novel cell death modality: cuproptosis. Cuproptosis exerts indispensable role cancer progression, considered promising strategy therapy. Cancer immunotherapy has gained extensive attention owing breakthroughs immune checkpoint blockade; furthermore, cuproptosis strongly connected modulation antitumor immunity. Thus, thorough recognition concerning mechanisms involved metabolism may facilitate improvement management. This review outlines cellular molecular characteristics links regulated modality with human cancers. We also current knowledge on complex effects immunity response. Furthermore, potential agents that elicit pathways are summarized. Lastly, we discuss influence induction tumor microenvironment as well challenges adding regulators therapeutic strategies beyond traditional
Язык: Английский
Процитировано
52
Molecular and Cellular Biochemistry, Год журнала: 2025, Номер unknown
Опубликована: Янв. 24, 2025
Язык: Английский
Процитировано
2
Frontiers in Pharmacology, Год журнала: 2023, Номер 14
Опубликована: Июль 26, 2023
Copper is an essential micronutrient that plays a critical role in many physiological processes. However, excessive copper accumulation cancer cells has been linked to tumor growth and metastasis. This review article explores the potential of targeting metabolism as promising strategy for treatment. Excessive associated with By disrupting homeostasis inducing cell death through copper-dependent mechanisms (cuproplasia cuprotosis, respectively), therapies can be developed improved efficacy reduced side effects. The discusses biological processes, such angiogenesis, immune response, redox homeostasis. Various approaches treatment are examined, including use enzymes, copper-based compounds, cuprotosis-related genes or proteins. also strategies like chelation therapy nanotechnology targeted delivery copper-targeting agents. understanding intricate network cuprotosis its interactions microenvironment system, new targets identified, leading outcomes. Overall, this comprehensive highlights significant effective approach treatment, while providing valuable insights into current state research field.
Язык: Английский
Процитировано
26
Frontiers in Immunology, Год журнала: 2024, Номер 15
Опубликована: Фев. 19, 2024
Background Myocardial infarction (MI) caused by severe coronary artery disease has high incidence and mortality rates, making its prevention treatment a central challenging aspect of clinical work for cardiovascular practitioners. Recently, researchers have turned their attention to novel mechanism cell death Cu 2+ , cuproptosis. Methods This study integrated data from three MI-related bulk datasets downloaded the Gene Expression Omnibus (GEO) database, identified 16 differentially expressed genes (DEGs) related cuproptosis taking intersection 6378 DEGs obtained differential analysis with 49 cuproptosis-related genes. Four hub genes, Dbt, Dlat, Ube2d1 Ube2d3, were screened out through random forest Lasso analysis. In group, showed low expression, while Ube2d3 exhibited expression. Results Focusing on subsequent functional studies, we confirmed expression in MI group qRT-PCR Western Blot detection after successful construction mouse model left anterior descending (LAD) ligation, further clarified correlation development detecting levels proteins. Moreover, vitro experiments, was be highly oxygen-glucose deprivation (OGD)-treated cardiomyocytes AC16. order clarify role knocked down OGD-treated AC16 cells, Ube2d3’s promoting hypoxia damage cells inducing cuproptosis, as evidenced MTT, TUNEL, LDH release Conclusion summary, our findings indicate that regulates affect progression MI.
Язык: Английский
Процитировано
12
Chemico-Biological Interactions, Год журнала: 2024, Номер 393, С. 110943 - 110943
Опубликована: Март 9, 2024
Язык: Английский
Процитировано
12
Molecular and Cellular Biochemistry, Год журнала: 2024, Номер unknown
Опубликована: Март 31, 2024
Язык: Английский
Процитировано
11
APOPTOSIS, Год журнала: 2024, Номер 29(7-8), С. 981 - 1006
Опубликована: Июнь 2, 2024
Язык: Английский
Процитировано
11
Mitochondrion, Год журнала: 2023, Номер 71, С. 1 - 16
Опубликована: Май 11, 2023
Язык: Английский
Процитировано
17
Journal of Cancer Research and Clinical Oncology, Год журнала: 2024, Номер 150(6)
Опубликована: Июнь 4, 2024
Abstract Background Butyrate is a common short-chain fatty acids (SCFA), and it has been demonstrated to regulate the development of breast cancer (BC), while underlying mechanism still unreported. Methods Gas chromatography was used measure amounts SCFA (acetate, propionate, butyrate) in feces. Cell viability measured by CCK-8 assay. The wound healing assay cell migration, transwell invasion. levels protein gene were determined western blot RT-qPCR assay, respectively. Results lower faecal samples from BC patients compared control samples. In cellular experiments, butyrate significantly suppressed viability, migration invasion T47D dose-dependent manner. animal effectively impeded growth tumors. Toll like receptor 4 (TLR4) highly expressed tumors patients. inhibited expression TLR4. addition, promoted cuproptosis-related genes including PDXK (pyridoxal kinase) SLC25A28 (solute carrier family 25 member 28), which lowly Importantly, overexpression TLR4 can reverses promotion prevention malignant biological behaviors cells. Conclusion summary, inhibits facilitating through inhibition Our investigation first identified connection among butyrate, progression. These findings may provide novel target for treatment BC.
Язык: Английский
Процитировано
8
Cell Communication and Signaling, Год журнала: 2024, Номер 22(1)
Опубликована: Июль 27, 2024
Abstract Copper is an important metal micronutrient, required for the balanced growth and normal physiological functions of human organism. Copper-related toxicity dysbalanced metabolism were associated with disruption intracellular respiration development various diseases, including cancer. Notably, copper-induced cell death was defined as cuproptosis which also observed in malignant cells, representing attractive anti-cancer instrument. Excess copper leads to aggregation lipoylation proteins toxic stress, ultimately resulting activation death. Differential expression cuproptosis-related genes detected tissues. Cuproptosis-related linked regulation oxidative immune responses, composition tumor microenvironment. Activation increased redox-metabolism-regulating genes, such ferredoxin 1 (FDX1), lipoic acid synthetase (LIAS), lipoyltransferase (LIPT1), dihydrolipoamide dehydrogenase (DLD), drolipoamide S-acetyltransferase (DLAT), pyruvate E1 subunit alpha (PDHA1), beta (PDHB)). Accordingly, copper-activated network suggested target cancer therapy. Mechanisms different cancers microenvironment are discussed this study. The analysis current findings indicates that therapeutic signaling, targets may provide effective tool improvement immunotherapy regimens. Graphical
Язык: Английский
Процитировано
7