Radiotherapy promotes cuproptosis and synergizes with cuproptosis inducers to overcome tumor radioresistance DOI Creative Commons
Guang Lei, Mingchuang Sun, Jun Cheng

и другие.

Cancer Cell, Год журнала: 2025, Номер unknown

Опубликована: Апрель 1, 2025

Язык: Английский

Breast cancer: pathogenesis and treatments DOI Creative Commons
Xin Xiong,

Lewei Zheng,

Yu‐Qiang Ding

и другие.

Signal Transduction and Targeted Therapy, Год журнала: 2025, Номер 10(1)

Опубликована: Фев. 18, 2025

Abstract Breast cancer, characterized by unique epidemiological patterns and significant heterogeneity, remains one of the leading causes malignancy-related deaths in women. The increasingly nuanced molecular subtypes breast cancer have enhanced comprehension precision treatment this disease. mechanisms tumorigenesis progression been central to scientific research, with investigations spanning various perspectives such as tumor stemness, intra-tumoral microbiota, circadian rhythms. Technological advancements, particularly those integrated artificial intelligence, significantly improved accuracy detection diagnosis. emergence novel therapeutic concepts drugs represents a paradigm shift towards personalized medicine. Evidence suggests that optimal diagnosis models tailored individual patient risk expected are crucial, supporting era oncology for cancer. Despite rapid advancements increasing emphasis on clinical comprehensive update summary panoramic knowledge related disease needed. In review, we provide thorough overview global status including its epidemiology, factors, pathophysiology, subtyping. Additionally, elaborate latest research into contributing progression, emerging strategies, long-term management. This review offers valuable insights Cancer Research, thereby facilitating future progress both basic application.

Язык: Английский

Процитировано

27

Advances in the study of disulfidptosis in digestive tract tumors DOI Creative Commons
Yue Chen, Dachuan Zhang, Huijuan Yang

и другие.

Discover Oncology, Год журнала: 2025, Номер 16(1)

Опубликована: Фев. 15, 2025

Disulfidptosis, a recently identified cell death mechanism, plays pivotal role in the development, progression, and treatment of digestive tract tumors, including gastric cancer, hepatocellular esophageal colorectal pancreatic cholangiocarcinoma, neuroendocrine which have high global incidence mortality rates. Analyzing expression disulfidptosis-related gene within tumor microenvironment enhances our understanding biology facilitates novel diagnostic therapeutic strategies. Research on immune infiltration checkpoints can identify targets linked to disulfidptosis, thereby improving immunotherapy efficacy. Targeting genes such as SLC7A11, are essential for maintaining glutathione levels regulating oxidative stress, may overcome chemoresistance enhance existing treatments. Disulfidptosis could complement current therapies it induces cytoskeletal collapse selective death, especially chemoresistant cancers. Additionally, like RPN1, NCKAP1 cancer correlate with poor prognosis, highlighting their potential prognostic biomarkers. Personalized medicine approaches utilizing biomarkers patients who would benefit from targeting stress regulation, leading more precise treatments improved outcomes. This review summarizes disulfidptosis mechanisms, advancements cancers, related response evaluation, targeted therapies, providing perspectives diagnosis personalized treatment.

Язык: Английский

Процитировано

3

Emerging mechanisms and promising approaches in pancreatic cancer metabolism DOI Creative Commons
Hao Wu,

Mengdi Fu,

Mengwei Wu

и другие.

Cell Death and Disease, Год журнала: 2024, Номер 15(8)

Опубликована: Авг. 1, 2024

Abstract Pancreatic cancer is an aggressive with a poor prognosis. Metabolic abnormalities are one of the hallmarks pancreatic cancer, and cells can adapt to biosynthesis, energy intake, redox needs through metabolic reprogramming tolerate nutrient deficiency hypoxic microenvironments. use glucose, amino acids, lipids as maintain malignant growth. Moreover, they also metabolically interact in tumour microenvironment change cell fate, promote progression, even affect immune responses. Importantly, changes at body level deserve more attention. Basic research clinical trials based on targeted therapy or combination other treatments full swing. A comprehensive in-depth understanding regulation will not only enrich mechanisms disease progression but provide inspiration for new diagnostic therapeutic approaches.

Язык: Английский

Процитировано

15

Sonodynamic Activated Nanoparticles with Glut1 Inhibitor and Cystine-containing Polymer Stimulate Disulfidptosis for Improved Immunotherapy in Bladder Cancer DOI Creative Commons
Ke Wang, Li Li,

Ganghao Liang

и другие.

Biomaterials, Год журнала: 2025, Номер 319, С. 123178 - 123178

Опубликована: Фев. 8, 2025

Язык: Английский

Процитировано

2

Synchronously Evoking Disulfidptosis and Ferroptosis via Systematical Glucose Deprivation Targeting SLC7A11/GSH/GPX4 Antioxidant Axis DOI

Mengsi Zhang,

Hao Zheng,

Xuanqi Zhu

и другие.

ACS Nano, Год журнала: 2025, Номер unknown

Опубликована: Апрель 3, 2025

Disulfidptosis and ferroptosis are recently identified programmed cell deaths for tumor therapy, both of which highly depend on the intracellular cystine/cysteine transformation cystine transporter solute carrier family 7 member 11/glutathione/glutathione peroxidase 4 (SLC7A11/GSH/GPX4) antioxidant axis. However, disulfidptosis usually asynchronous due to opposite effect transport them. Herein, systematic glucose deprivation, by inhibiting upstream uptake promoting downstream consumption, is proposed synchronously evoke ferroptosis. As an example, Au nanodots Fe-apigenin (Ap) complexes coloaded FeOOH nanoshuttles (FeOOH@Fe-Ap@Au NSs) employed regulate SLC7A11/GSH/GPX4 axis performing disulfidptosis- ferroptosis-mediated therapy synchronously. In this scenario, exhibit oxidase-like activity when consuming massive glucose. Meanwhile, Ap can inhibit downregulating 1, depriving fundamentally. The systematical deprivation limits supplement NADPH suppresses axis, thus solving contradiction addition, efficient delivery exogenous iron ions FeOOH@Fe-Ap@Au NSs self-supplied H2O2 through nanodots-catalytic oxidation facilitate Fenton reaction therewith help amplify a result synchronous occurrence ferroptosis, good efficacy in ovarian cancer therapeutic model.

Язык: Английский

Процитировано

1

Cuproptosis, the novel type of oxidation-induced cell death in thoracic cancers: can it enhance the success of immunotherapy? DOI Creative Commons

Ruiwen Zhao,

Olga Sukocheva, Edmund C. M. Tse

и другие.

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

8

Theoretical Framework and Emerging Challenges of Lipid Metabolism in Cancer DOI Creative Commons
Qiuying Gu, Yuan Wang, Ping Yi

и другие.

Seminars in Cancer Biology, Год журнала: 2024, Номер unknown

Опубликована: Дек. 1, 2024

Elevated lipid metabolism is one of hallmarks malignant tumors. Lipids not only serve as essential structural components biological membranes but also provide energy and substrates for the proliferation cancer cells tumor growth. Cancer meet their needs by coordinating processes absorption, synthesis, transport, storage, catabolism. As research in this area continues to deepen, numerous new discoveries have emerged, making it crucial scientists stay informed about developments metabolism. In review, we first discuss relevant concepts theories or assumptions that help us understand -based therapies. We then systematically summarize latest advancements including mechanisms, novel targets, up-to-date pre-clinical clinical investigations anti-cancer treatment with targeted drugs. Finally, emphasize emerging directions therapeutic strategies, future prospective challenges. This review aims insights guidance field

Язык: Английский

Процитировано

8

Multiomic Landscape of Primary Hypothyroidism Induced by Subchronic Exposure to Low-Dose Novel PFOS Substitute OBS in Human and Murine Models DOI
Yang Wang,

Ke Ma,

Supeng Yin

и другие.

Environmental Science & Technology, Год журнала: 2025, Номер unknown

Опубликована: Апрель 3, 2025

Sodium p-perfluorous nonenoxybenzenesulfonate (OBS) as a novel surrogate for perfluorooctanesulfonate (PFOS) has been extensively utilized in industrial manufacturing and daily life. However, studies on OBS-induced environmental health risks of obstructive biosynthesis are currently limited, particularly the risk thyroid diseases. Following construction vivo (mouse) vitro (normal human primary thyrocytes) models subchronic low-dose OBS exposure, we explored thyroid-disrupting effects through multiomics approaches experimental validations. Our results showed that exposure to low doses led hypothyroidism mice, presenting with reduced number functional abnormalities thyrocytes. Further assays confirmed disulfidptosis, newly discovered form programmed cell death, Meanwhile, remarkably suppressed hormone synthesis pathways mouse The charted multiomic landscape mammals revealed toxicity endocrine-disrupting properties OBS, suggesting it is not safe alternative PFOS.

Язык: Английский

Процитировано

1

PSAT1 impairs ferroptosis and reduces immunotherapy efficacy via GPX4 hydroxylation DOI

Peixiang Zheng,

Z. Hu, Shen Yu-li

и другие.

Nature Chemical Biology, Год журнала: 2025, Номер unknown

Опубликована: Апрель 25, 2025

Язык: Английский

Процитировано

1

Targeting Ferroptosis as an Advance Strategy in Cancer Therapy DOI
Tobias Achu Muluh, Qianqian Fu,

Xiaojiao Ai

и другие.

Antioxidants and Redox Signaling, Год журнала: 2024, Номер 41(10-12), С. 616 - 636

Опубликована: Июль 3, 2024

This study innovates by systematically integrating the molecular mechanisms of iron death and its application in cancer therapy. By deeply analyzing interaction between tumor microenvironment, provides a new theoretical basis for treatment directions developing more effective strategies. In addition, points to critical issues barriers that need be addressed future research, providing valuable insights into use clinical translation.

Язык: Английский

Процитировано

6