Utilize este identificador para referenciar este registo: https://hdl.handle.net/1822/90073

TítuloSmart mitochondria-specific anchored gold-based nanosystem for integration of tumor imaging and treatment
Autor(es)Yin, Xuelian
Zhan, Lin
Ding, Lin
Chen, Xuerui
Zhang, Junfeng
Li, Chenchen
Zhang, Yuxi
Khan, Murad
Reis, R. L.
Wang, Yanli
Palavras-chaveFluorescence imaging
Mitochondria-specific anchored
Reactive oxygen species
Tumor targeting
DataFev-2023
EditoraWiley
RevistaAdvanced Materials Technologies
CitaçãoYin X. L., Zhan L., Ding L., Chen X. R., Zhang J. F., Li C. C., Zhang Y. X., Khan M., Reis R. L., Wang Y. L. Smart Mitochondria-Specific Anchored Gold-based Nanosystem for Integration of Tumor Imaging and Treatment, Advanced Materials Technologies, 2023, Vol. 8, Issue 10, pp. 2201929, doi:https://doi.org/10.1002/admt.202201929
Resumo(s)Although recent advances have been made in improving the efficacy of photodynamic therapy, efficient therapeutic approaches based on reactive oxygen species (ROS) are needed, particularly mitochondria-specific targeting of nanomaterials that can alter the internal environment of organelles. Herein, we report the facile synthesis of mitochondria-specific anchored nano-complexes (AG-CNP) comprised of a skeleton of gold and carbon atoms for cancer therapy. Compared to the effects of gold nanoclusters (Au NCs), AG-CNP shows enhanced fluorescence imaging effects, which can be used for tumor monitoring. AG-CNP targets the mitochondria and increases ROS damage in cancer cells. After treatment with AG-CNP, the tumor inhibition rate reaches 70.94%, which is 25.98% and 36.91% higher than that of free doxorubicin (DOX) and gemcitabine (Gem), respectively. Studying the mechanism of AG-CNP inhibiting cancer shows that AG-CNP can promote tumor cells to produce excessive ROS by overexpressing P53 and increasing the number of apoptotic cancer cells, which is caused by overexpression of Caspase1 that was closely related to cell apoptosis. AG-CNP is a promising anticancer drug that targets the mitochondria in vivo to trigger excessive ROS production in tumor cells and inhibit tumor growth.
TipoArtigo
URIhttps://hdl.handle.net/1822/90073
DOI10.1002/admt.202201929
ISSN2365-709X
Versão da editorahttps://onlinelibrary.wiley.com/doi/10.1002/admt.202201929
Arbitragem científicayes
AcessoAcesso aberto
Aparece nas coleções:3B’s - Artigos em revistas/Papers in scientific journals


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