International Journal of Biological Macromolecules, Год журнала: 2024, Номер unknown, С. 138760 - 138760
Опубликована: Дек. 1, 2024
Язык: Английский
International Journal of Biological Macromolecules, Год журнала: 2024, Номер unknown, С. 138760 - 138760
Опубликована: Дек. 1, 2024
Язык: Английский
Pharmaceuticals, Год журнала: 2025, Номер 18(3), С. 325 - 325
Опубликована: Фев. 26, 2025
The emergence of nanotechnology in medicine, particularly using iron oxide nanoparticles (IONPs), may impact cancer treatment strategies. IONPs exhibit unique properties, such as superparamagnetism, biocompatibility, and ease surface modification, making them ideal candidates for imaging, therapeutic interventions. Their application targeted drug delivery, especially with traditional chemotherapeutic agents like cisplatin, has shown potential overcoming limitations low bioavailability systemic toxicity chemotherapies. Moreover, IONPs, by releasing ions, can induce ferroptosis, a form iron-dependent cell death, which offers promising pathway to reverse radio- chemoresistance therapy. In particular, demonstrate significant radiosensitisers, enhancing the effects radiotherapy promoting reactive oxygen species (ROS) generation, lipid peroxidation, modulating tumour microenvironment stimulate antitumour immune responses. This review explores multifunctional roles radiosensitisation through ferroptosis induction, highlighting their promise advancing head neck cancers. Additional research is crucial fully addressing clinical settings, offering novel approach personalised treatment.
Язык: Английский
Процитировано
1Cancer Drug Resistance, Год журнала: 2024, Номер unknown
Опубликована: Окт. 25, 2024
NFE2-like basic leucine zipper transcription factor 2 (NFE2L2, also known as NRF2), is a key in the cellular defense against oxidative stress, playing crucial role cancer cell survival and resistance to therapies. This review outlines current knowledge on link between NFE2L2 ferroptosis - form of regulated death characterized by iron-dependent lipid peroxidation within cells. While activation can protect normal cells from damage, its overexpression contributes drug upregulating antioxidant defenses inhibiting ferroptosis. We delve into molecular pathways ferroptosis, highlighting involvement target genes, such
Язык: Английский
Процитировано
8Frontiers in Pharmacology, Год журнала: 2024, Номер 15
Опубликована: Июль 15, 2024
Metastatic hepatocellular carcinoma (HC) is a serious health concern. The stemness of cancer stem cells (CSCs) key driver for HC tumorigenesis, apoptotic resistance, and metastasis, functional mitochondria are critical its maintenance. Cuproptosis Cu-dependent non-apoptotic pathway (mitochondrial dysfunction) via inactivating mitochondrial enzymes (pyruvate dehydrogenase "PDH" succinate "SDH"). To effectively treat metastatic HC, it necessary to induce selective cuproptosis (for halting genes) with oxidative imbalance increasing cell susceptibility inducing non-CSCs death). Herein, two types Cu oxide nanoparticles (Cu
Язык: Английский
Процитировано
5Frontiers in Oncology, Год журнала: 2025, Номер 15
Опубликована: Янв. 30, 2025
Cell death mechanisms are broadly classified into accidental cell (ACD) and regulated (RCD). ACD such as necrosis, is an uncontrolled, process, while RCD tightly by specific signaling pathways molecular mechanisms. Tumor cells characterized their ability to evade sustain uncontrolled proliferation. The failure of programmed a key contributor tumor initiation, progression, resistance cancer therapies. Traditionally, research has focused primarily on apoptosis the dominant form in cancer. However, emerging evidence highlights importance other non-apoptotic forms RCD, pyroptosis, ferroptosis, necroptosis, parthanatos, tumorigenesis treatment response. These gaining attention for potential roles overcoming therapy resistance. In this review, we will discuss recent advances study malignant tumors explore therapeutic implications, offering insights new targets strategies.
Язык: Английский
Процитировано
0Journal of Gastroenterology, Год журнала: 2025, Номер unknown
Опубликована: Янв. 31, 2025
Язык: Английский
Процитировано
0International Immunopharmacology, Год журнала: 2025, Номер 155, С. 114597 - 114597
Опубликована: Апрель 15, 2025
Язык: Английский
Процитировано
0Acta Materia Medica, Год журнала: 2025, Номер 4(3)
Опубликована: Янв. 1, 2025
Tumor ferroptosis, a regulated form of cell death driven by iron-dependent lipid peroxidation, has emerged as promising therapeutic strategy for combating cancers, particularly in cases involving cancer stem cells (CSCs) and drug resistance. In recent years nanomaterial-based approaches have gained significant attention the potential to selectively induce ferroptosis while sparing normal tissues. This review aims provide comprehensive overview current state-of-the-art utilizing nanomaterials targeting tumor with specific focus on application eradicating CSCs overcoming resistance mechanisms. The molecular mechanisms underlying induction nanomaterials, unique properties functionalities various nanomaterial platforms, strategies using nanoferroptosis will be discussed. addition, preclinical clinical evidence supporting efficacy platforms evaluated. Furthermore, challenges future perspectives development translation nanoferroptosis-based therapies precision treatment highlighted.
Язык: Английский
Процитировано
0Nanomedicine, Год журнала: 2025, Номер unknown, С. 1 - 14
Опубликована: Май 16, 2025
Targeting cancer stem cells (CSCs)-mediated aggressive features of non-small cell lung (NSCLC) is a promising anticancer approach. This can be accomplished via suppressing critical mediators, such as functional mitochondria, aldehyde dehydrogenase (ALDH)1A, and telomere protectors (telomerase reverse transcriptase (TERT) repeat binding factor (TRF)1). Copper nanocomplexes (diethyldithiocarbamate (DE)-Cu4O3 nanoparticles (NPs) DE-Cu NPs) were prepared using the simplest green chemistry method assessed for inducing mitochondrial dysfunction-dependent non-apoptotic pathway (cuproptosis) repressing CSC markers. DE-Cu4O3 NPs had higher growth inhibition NSCLC (A549, H520, H1299) spheroids than NPs. uptake rate prooxidant effect resulting in lower membrane potential DNA copy number, well stronger telomerase ALDH1A caused dramatic redox imbalance lowering AKT (activator stabilizers stemness)-mediated repression TERT TRF1 protein levels phosphorylated NF-κB subunit (p65) led to collapsing telomeres, evidenced by downregulating regulators confocal microscopy. In animal study, this active nanocomplex revealed powerful selective therapeutic tumor-targeting effects, with no evidence toxicity healthy tissues. deemed nanomedicine NSCLC.
Язык: Английский
Процитировано
0Interdisciplinary cancer research, Год журнала: 2024, Номер unknown
Опубликована: Янв. 1, 2024
Язык: Английский
Процитировано
1International Journal of Biological Macromolecules, Год журнала: 2024, Номер unknown, С. 138760 - 138760
Опубликована: Дек. 1, 2024
Язык: Английский
Процитировано
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