Antioxidants in cancer therapy mitigating lipid peroxidation without compromising treatment through nanotechnology DOI Creative Commons
Daniel Ejim Uti, Item Justin Atangwho, Esther Ugo Alum

и другие.

Discover Nano, Год журнала: 2025, Номер 20(1)

Опубликована: Апрель 24, 2025

Cancer treatments often exploit oxidative stress to selectively kill tumour cells by disrupting their lipid peroxidation membranes and inhibiting antioxidant enzymes. However, plays a dual role in cancer progression, acting as both promoter suppressor. Balancing through therapy remains challenge, excessive activity may compromise the efficacy of chemotherapy radiotherapy. This review explores antioxidants mitigating while maintaining treatment efficacy. It highlights recent advancements nanotechnology-based targeted delivery optimize therapeutic outcomes. A comprehensive literature was conducted using reputable databases, including PubMed, Scopus, Web Science, ScienceDirect. The search focused on publications from past five years (2020-2025), supplemented relevant studies earlier years. Keywords such "antioxidants," "lipid peroxidation," "nanotechnology therapy," "oxidative stress" were utilized. Relevant articles critically analysed, graphical illustrations created. Emerging evidence suggests that nanoparticles, liposomes, polymeric metal-organic frameworks, others, can effectively encapsulate control release minimizing systemic toxicity. Stimuli-responsive carriers with tumour-specific targeting mechanisms further enhance delivery. Studies indicate these strategies help preserve normal cells, mitigate stress-related damage, improve challenges bioavailability, stability, potential interactions standard therapies remain. Integrating nanotechnology antioxidant-based interventions presents promising approach for optimizing therapy. Future research should focus refining modulation strategies, assessing profiles during treatment, employing biomarkers determine optimal dosing. balanced use adverse effects.

Язык: Английский

Harnessing the FOXO-SIRT1 axis: insights into cellular stress, metabolism, and aging DOI
Saurabh Gupta, Muhammad Afzal, Neetu Agrawal

и другие.

Biogerontology, Год журнала: 2025, Номер 26(2)

Опубликована: Фев. 26, 2025

Язык: Английский

Процитировано

0
Targeting p70S6K1 Inhibits Glycated Albumin-Induced Triple-Negative Breast Cancer Cell Invasion and Overexpression of Galectin-3, a Potential Prognostic Marker in Diabetic Patients with Invasive Breast Cancer DOI Creative Commons

Fatimah Alanazi,

Abdulmonem A. Alsaleh, Mariam K. Alamoudi

и другие.

Biomedicines, Год журнала: 2025, Номер 13(3), С. 612 - 612

Опубликована: Март 3, 2025

Background: There is an urgent need to identify new biomarkers for early diagnosis and development of therapeutic strategies diabetes mellitus (DM) patients who have invasive breast cancer (BC). We previously reported the increased activated form 70 kDa ribosomal protein S6 kinase 1 (phospho-p70S6K1) in a triple-negative BC (TNBC) cell line MDA-MB-231 exposed glycated albumin (GA) ductal carcinoma tissues from T2DM patients, compared untreated cells their non-diabetic counterparts, respectively. Objective: aimed explore function p70S6K1 GA-promoted TNBC progression. Methods: By employing small interference (si)RNA technology or blocking its activity using specific pharmacological inhibitor, we monitored invasion Transwell® inserts expression levels signaling proteins cancer-related Western blot. Results: In silico analysis revealed that high mRNA were associated with unfavorable prognosis progression advanced stages DM patients. The downregulation/blockade inhibited phosphorylation ERK1/2, downstream effector, key oncogenic protein, suppression GA-upregulated proteins, including enolase-2, capping CapG, galectin-3, cathepsin D, was observed after downregulation/blockade. Further validation analyses gene galectin-3 resulting poor overall survival disease-free survival. Conclusions: Targeting may present valuable strategy, while could serve as potential prognostic biomarker

Язык: Английский

Процитировано

0
Antioxidants in cancer therapy mitigating lipid peroxidation without compromising treatment through nanotechnology DOI Creative Commons
Daniel Ejim Uti, Item Justin Atangwho, Esther Ugo Alum

и другие.

Discover Nano, Год журнала: 2025, Номер 20(1)

Опубликована: Апрель 24, 2025

Cancer treatments often exploit oxidative stress to selectively kill tumour cells by disrupting their lipid peroxidation membranes and inhibiting antioxidant enzymes. However, plays a dual role in cancer progression, acting as both promoter suppressor. Balancing through therapy remains challenge, excessive activity may compromise the efficacy of chemotherapy radiotherapy. This review explores antioxidants mitigating while maintaining treatment efficacy. It highlights recent advancements nanotechnology-based targeted delivery optimize therapeutic outcomes. A comprehensive literature was conducted using reputable databases, including PubMed, Scopus, Web Science, ScienceDirect. The search focused on publications from past five years (2020-2025), supplemented relevant studies earlier years. Keywords such "antioxidants," "lipid peroxidation," "nanotechnology therapy," "oxidative stress" were utilized. Relevant articles critically analysed, graphical illustrations created. Emerging evidence suggests that nanoparticles, liposomes, polymeric metal-organic frameworks, others, can effectively encapsulate control release minimizing systemic toxicity. Stimuli-responsive carriers with tumour-specific targeting mechanisms further enhance delivery. Studies indicate these strategies help preserve normal cells, mitigate stress-related damage, improve challenges bioavailability, stability, potential interactions standard therapies remain. Integrating nanotechnology antioxidant-based interventions presents promising approach for optimizing therapy. Future research should focus refining modulation strategies, assessing profiles during treatment, employing biomarkers determine optimal dosing. balanced use adverse effects.

Язык: Английский

Процитировано

0