
Seminars in Cancer Biology, Journal Year: 2024, Volume and Issue: 106-107, P. 123 - 142
Published: Sept. 30, 2024
Language: Английский
Seminars in Cancer Biology, Journal Year: 2024, Volume and Issue: 106-107, P. 123 - 142
Published: Sept. 30, 2024
Language: Английский
Advanced Therapeutics, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 3, 2025
Abstract Copper plays a pivotal role in human physiology, particularly oncology, acting both as facilitator of progression and also potential avenue for advanced therapeutic approaches. Maintaining copper homeostasis is crucial. The dysregulation implicated tumor growth through its involvement critical processes angiogenesis, proliferation, metastasis. elevation level the microenvironment (TME) activates oncogenic pathways to drive neovascularization sustained malignancies. However, same reliance on offers unique weakness that can be leveraged innovative interventions. recent advances nanomedicine enable synthesis nanostructures help modulate with precision offering multifaceted approaches copper‐based cancer therapy controlled release mechanism, optimized structures induce cuproptosis, selective eradication cells minimum systemic toxicity. This review explores dual biology, emphasizing contribution tumors emerging application targeted therapy. highlights harnessing therapies their transformative from bench bed side novel, highly effective, clinical safety.
Language: Английский
Citations
1Advanced Science, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 20, 2025
Abstract Cuproptosis, a recently defined copper‐dependent cell death pathway, remains largely unexplored in tumor therapies, particularly breast cancer. This study demonstrates that triple‐negative cancer (TNBC) bears relatively elevated copper levels and exhibits resistance to cuproptosis. Mechanistically, activates the AKT signaling which inhibits ferredoxin‐1 (FDX1), key regulator of AKT1‐mediated FDX1 phosphorylation not only abrogates FDX1‐induced cuproptosis aerobic respiration but also promotes glycolysis. Consequently, combination AKT1 inhibitors ionophores synergistically alleviate TNBC tumorigenesis both vitro vivo. In summary, findings reveal crucial mechanism underlying suggest potential therapeutic approach for TNBC.
Language: Английский
Citations
1Molecular Carcinogenesis, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 23, 2025
ABSTRACT Cuproptosis is a form of programmed cell death dependent on mitochondrial respiration and crucial in cancer treatment. The study attempted to screen cuproptosis‐associated genes colorectal (CRC) reveal regulatory pathways. Weighted gene co‐expression network analysis (WGCNA) was applied the modules based expression CRC patients. were screened at intersection cuproptosis data set. RNA sequencing performed assess transcriptome changes, followed by functional enrichment analyses potential Ferredoxin 1 (FDX1) knocked down vivo vitro experiments investigate effects FDX1 knockdown progression cuproptosis. found as highly expressed tumor cells. Knockdown regulated cells, inhibited growth, migration invasion. We 1956 upregulated DEGs 2201 downregulated si‐FDX1 which mainly enriched mitogen‐activated protein kinase (MAPK) signaling pathway, necrosis factor (TNF) pathway Hippo pathway. increasing levels dihydrolipoamide S‐succinyltransferase (DLST), lipoic acid synthetase (LIAS) phosphorylation Yes‐associated (pYAP)/YAP, transcriptional coactivator with PDZ‐binding domain (TAZ). inhibitor GA‐017 blocked this process. Knocking mediating shed new insights into development biomarkers for
Language: Английский
Citations
1Materials Horizons, Journal Year: 2024, Volume and Issue: 11(18), P. 4275 - 4310
Published: Jan. 1, 2024
This comprehensive review systematically summarizes the intrinsic mechanism of different metal ion (such as Fe 3+ /Fe 2+ , Cu /Cu + Ca Zn Mn Na /K and Mg )-mediated interference therapies their research progress in cancer treatment.
Language: Английский
Citations
7Seminars in Cancer Biology, Journal Year: 2024, Volume and Issue: 106-107, P. 123 - 142
Published: Sept. 30, 2024
Language: Английский
Citations
7