SBFI26 induces triple‐negative breast cancer cells ferroptosis via lipid peroxidation DOI Creative Commons
Gang He, Yiyuan Zhang,

Yanjiao Feng

et al.

Journal of Cellular and Molecular Medicine, Journal Year: 2024, Volume and Issue: 28(7)

Published: March 22, 2024

Abstract SBFI26, an inhibitor of FABP5, has been shown to suppress the proliferation and metastasis tumour cells. However, underlying mechanism by which SBFI26 induces ferroptosis in breast cancer cells remains largely unknown. Three cell lines were treated with CCK‐8 assessed cytotoxicity. Transcriptome was performed on Illumina platform verified qPCR. Western blot evaluated protein levels. Malondialdehyde (MDA), total superoxide dismutase (T‐SOD), Fe, glutathione (GSH) oxidized (GSSG) measured. induced death time‐ dose‐dependent, a more significant inhibitory effect MDA‐MB‐231 Fer‐1, GSH Vitamin C attenuated effects but not erastin. RNA‐Seq analysis revealed that treatment significantly enriched differentially expressed genes related ferroptosis. Furthermore, increased intracellular MDA, iron ion, GSSG levels while decreasing T‐SOD, (T‐GSH), levels.SBFI26 dose‐dependently up‐regulates expression HMOX1 ALOX12 at both gene levels, promoting Similarly, it increases SAT1, ALOX5, ALOX15, ALOXE3 CHAC1 that, downregulating NFE2L2 inhibit leads cellular accumulation fatty acids, triggers excess ferrous ions subsequent lipid peroxidation for inducing

Language: Английский

The roles of ferroptosis in cancer: Tumor suppression, tumor microenvironment, and therapeutic interventions DOI Open Access
Guang Lei, Li Zhuang, Boyi Gan

et al.

Cancer Cell, Journal Year: 2024, Volume and Issue: 42(4), P. 513 - 534

Published: April 1, 2024

Language: Английский

Citations

116

Targeting immunogenic cell stress and death for cancer therapy DOI
Lorenzo Galluzzi, Emma Guilbaud,

Darby Schmidt

et al.

Nature Reviews Drug Discovery, Journal Year: 2024, Volume and Issue: 23(6), P. 445 - 460

Published: April 15, 2024

Language: Английский

Citations

82

Roles of Oxidative Stress in Synaptic Dysfunction and Neuronal Cell Death in Alzheimer’s Disease DOI Creative Commons
Germán Plascencia‐Villa, George Perry

Antioxidants, Journal Year: 2023, Volume and Issue: 12(8), P. 1628 - 1628

Published: Aug. 17, 2023

Alzheimer’s disease (AD) is a brain disorder that progressively undermines memory and thinking skills by affecting the hippocampus entorhinal cortex. The main histopathological hallmarks of AD are presence abnormal protein aggregates (Aβ tau), synaptic dysfunction, aberrant proteostasis, cytoskeletal abnormalities, altered energy homeostasis, DNA RNA defects, inflammation, neuronal cell death. However, oxidative stress or damage also evident commonly overlooked considered consequence advancement dementia symptoms. control onset linked to activity amyloid-β peptide, which may serve as both antioxidant pro-oxidant molecules. Furthermore, correlated with proteins, nucleic acids, lipids in vulnerable populations, ultimately lead death through different molecular mechanisms. By recognizing an integral feature AD, alternative therapeutic preventive interventions developed tested potential complementary therapies for this devastating neurodegenerative disease.

Language: Английский

Citations

58

Glutathione‐Scavenging Celastrol‐Cu Nanoparticles Induce Self‐Amplified Cuproptosis for Augmented Cancer Immunotherapy DOI
Sheng Lü, Yifan Li, Yingjie Yu

et al.

Advanced Materials, Journal Year: 2024, Volume and Issue: 36(35)

Published: June 27, 2024

Cuproptosis is a novel copper-dependent programmed cell death. The efficacy of cuproptosis highly dependent on intracellular copper accumulation and counteracted by high level glutathione (GSH) in tumor cells. Here, this work develops self-amplified nanoparticles (Cel-Cu NP) using celastrol (Cel), natural product isolated from medical plant. In Cel-Cu NP, Cel serves as versatile ionophore, exhibiting an ideal coordination capacity toward ions without compromising the induction. Notably, can simultaneously scavenge GSH content to amplify cuproptosis. Moreover, further activates immunogenic death (ICD) elicit robust immune response. Combining with checkpoint blockade, NP effectively eradicates metastatic tumors mouse lung metastasis model. This study provides efficient nanomedicine inducing for immunotherapy.

Language: Английский

Citations

44

Multi drug resistance in Colorectal Cancer- approaches to overcome, advancements and future success DOI Creative Commons
Sumel Ashique, Mithun Bhowmick, Radheshyam Pal

et al.

Advances in Cancer Biology - Metastasis, Journal Year: 2024, Volume and Issue: 10, P. 100114 - 100114

Published: Jan. 17, 2024

A significant obstacle to treating cancer is multidrug resistance (MDR), which the capacity of cancerous cells develop both traditional and cutting-edge chemotherapeutic treatments. Following initial discovery that cellular pumps reliant on ATP were root chemotherapy resistance, more research has revealed involvement additional mechanisms, including increased drug metabolism, reduced entry, compromised apoptotic pathways. Numerous projects have focused MDR, innumerable been conducted better understand MDR methods mitigate its consequences. Multidrug (MDR) a key challenge in cancer. 90% cancer-related fatalities are brought by tumor metastasis recurrence, possible with MDR. Drug influenced diverse internal extrinsic variables, genetic epigenetic changes, efflux systems, DNA repair apoptosis, autophagy. In this review paper, we list potential hazards associated therapy general, primarily developing theory for colorectal particular. We discussed unique instance malignancies generally 5-fluorouracil, curcumin, lipids as viable options condition. The use nanotechnology (mainly nanoparticles) facilitated vitro well vivo efficacy during preclinical phases, summarized below, allowing thorough investigation cancers pancreatic carcinomas their translation following clinical trials.

Language: Английский

Citations

43

Metabolic cell death in cancer: ferroptosis, cuproptosis, disulfidptosis, and beyond DOI Creative Commons
Chao Mao, Min Wang, Li Zhuang

et al.

Protein & Cell, Journal Year: 2024, Volume and Issue: 15(9), P. 642 - 660

Published: Feb. 29, 2024

Abstract Cell death resistance represents a hallmark of cancer. Recent studies have identified metabolic cell as unique forms regulated resulting from an imbalance in the cellular metabolism. This review discusses mechanisms death—ferroptosis, cuproptosis, disulfidptosis, lysozincrosis, and alkaliptosis—and explores their potential cancer therapy. Our underscores complexity pathways offers insights into innovative therapeutic avenues for treatment.

Language: Английский

Citations

42

Bioactive Layered Double Hydroxides for Synergistic Sonodynamic/Cuproptosis Anticancer Therapy with Elicitation of the Immune Response DOI
Wei Tang, Jie Wu, Li Wang

et al.

ACS Nano, Journal Year: 2024, Volume and Issue: 18(15), P. 10495 - 10508

Published: April 1, 2024

Sonodynamic therapy (SDT) has promising application prospects in tumor therapy. However, SDT does not eradicate metastatic tumors. Herein, Cu-substituted ZnAl ternary layered double hydroxide nanosheets (ZCA NSs) were developed as both sonosensitizers and copper nanocarriers for synergistic SDT/cuproptosis cancer An optimized electronic structure more conducive to the sonodynamic process was obtained from ZCA NSs via Jahn–Teller effect induced by introduction of Cu2+, synthesized regulated intricate microenvironment (TME) depleting endogenous glutathione (GSH) amplify oxidative stress further enhanced performance. Furthermore, cuproptosis evoked intracellular overload Cu2+ amplified SDT, leading irreversible proteotoxicity. In vitro results showed that such synergetic triggered immunogenic cell death (ICD) promoted maturation dendritic cells (DCs). as-synthesized NS-mediated thoroughly eradicated vivo solid tumors simultaneously elicited antitumor immunity suppress lung liver metastasis. Overall, this work established a nanoplatform with satisfactory immunity.

Language: Английский

Citations

38

A Vacancy‐Engineering Ferroelectric Nanomedicine for Cuproptosis/Apoptosis Co‐Activated Immunotherapy DOI

Yaqian Du,

Xudong Zhao, Fei He

et al.

Advanced Materials, Journal Year: 2024, Volume and Issue: 36(30)

Published: May 4, 2024

Abstract Low efficacy of immunotherapy due to the poor immunogenicity most tumors and their insufficient infiltration by immune cells highlights importance inducing immunogenic cell death activating system for achieving better treatment outcomes. Herein, ferroelectric Bi 2 CuO 4 nanoparticles with rich copper vacancies (named BCO‐V Cu ) are rationally designed engineered ferroelectricity‐enhanced apoptosis, cuproptosis, subsequently evoked immunotherapy. In this structure, suppressed recombination electron–hole pairs band bending polarization lead high catalytic activity, triggering reactive oxygen species bursts apoptosis. The fragments produced apoptosis serve as antigens activate T cells. Moreover, generated charge catalysis, nanomedicine can act “a smart switch” open membrane, promote nanomaterial endocytosis, shut down + outflow pathway evoke thus a strong response is triggered reduced content adenosine triphosphate. Ribonucleic acid transcription tests reveal pathways related activation. Thus, study firstly demonstrates feasible strategy enhancing using single semiconductor‐induced cuproptosis.

Language: Английский

Citations

38

A Copper/Ferrous‐Engineering Redox Homeostasis Disruptor for Cuproptosis/Ferroptosis Co‐Activated Nanocatalytic Therapy in Liver Cancer DOI
Xiaoling Zhang, Jiuxin Zhu,

Sihao Wang

et al.

Advanced Functional Materials, Journal Year: 2024, Volume and Issue: 34(37)

Published: April 25, 2024

Abstract Cuproptosis and ferroptosis hold great promise for overcoming apoptotic resistance in liver cancer based on their unique metal‐driven cell death modalities. However, insufficient intracellular copper iron concentration, complicated tumor microenvironment (TME), unclear cross‐regulatory mechanisms between cuproptosis ferroptosis, severely restrict the therapeutic performance. Herein, copper‐doped hollow Prussian blue (CHP) nanozymes are rationally designed loading photosensitizer indocyanine green (ICG) O 2 ‐saturated perfluorohexane (PFH), denoted as ‐PFH@CHPI nanoparticles, to induce ferroptosis. In response specific TME, CHP can synergistically catalyze Fenton reactions consume endogenous glutathione, leading accumulation of reactive oxygen species. Upon near‐infrared irradiation, ‐PFH@CHPI‐enabled photothermal effect simultaneously accelerate catalytic trigger release photodynamic therapy promote oxidative stress. Notably, be effectively activated through Cu + ‐mediated dihydrolipoamide S‐acetyltransferase aggregation Fe–S cluster protein loss. Concurrently, tilt redox balance is favorable lipid peroxidation glutathione peroxidase 4 inactivation, resulting an augmented effect. Mechanistically, stress‐boosted jointly disrupt mitochondrial metabolism, which turn exacerbates stress, thus realizing a mutually enhanced This work may provide new guidance utilizing copper/ferrous‐engineering cuproptosis/ferroptosis synergetic therapy.

Language: Английский

Citations

29

Gasdermin and MLKL necrotic cell death effectors: Signaling and diseases DOI Creative Commons
Kate E. Lawlor, James M. Murphy, James E. Vince

et al.

Immunity, Journal Year: 2024, Volume and Issue: 57(3), P. 429 - 445

Published: March 1, 2024

Language: Английский

Citations

21