Tumor microenvironment-activated, immunomodulatory nanosheets loaded with copper(II) and 5-FU for synergistic chemodynamic therapy and chemotherapy

Advances in H2O2-supplying materials for tumor therapy: synthesis, classification, mechanisms, and applications

“…Abundant intracellular copper will lead to oligomerization of lipoylated dihydrolipoamide S -acetyltransferase and dysfunction of the mitochondrial tricarboxylic acid cycle in cancer cells. 176 CuO 2 could release Cu 2+ in the tumor acidic environment. 177 Cu 2+ is reduced to Cu + and participates in Fenton-like reactions while consuming GSH to provide a convenient environment for CDT.…”

Cuproptosis in cancer: biological implications and therapeutic opportunities

“…Within tumor tissues, E-C@DOX NPs not only induce tumor cell cuproptosis but also inhibit the signaling pathways associated with tumor cell stemness and survival, enhance mitochondrial damage, thereby suppressing ATP-dependent drug efflux pathways and reversing DOX resistance in breast cancer [ 207 ]. LDH/HA/5-FU nanosheets can specifically target tumor cells and release Cu 2+ and 5-FU, thereby inducing cuproptosis and apoptosis in tumor cells, exhibiting outstanding inhibitory effects on tumors [ 208 ].…”

“…Furthermore, GOx@(Cu(tz)) effectively inhibited tumor growth in athymic mice bearing 5637 bladder tumors [ 205 ] DSF@PEG/Cu-HMSNs DSF, PEG, Cu 2+ , hollow mesoporous silica nanoparticles (HMSNs) Mild acidic TME This nanosystem effectively curbed the growth of 4T1 cell-derived tumors in female BALB/C nude mice [ 206 ] E-C@DOX NPs Cu 2+ ; ellagic acid (EA); DOX; chondroitin sulfate (CS) GSH; low-pH environment; CS-mediated internalization E-C@DOX NPs inhibits tumor cell stemness and cell survival-related pathways, while working in tandem with Cu ions to damage mitochondria and induce cuproptosis, thereby suppressing the ATP-dependent drug efflux pathway and reversing DOX resistance [ 207 ] LDH/HA/5-FU nanosheets 5-FU; copper–aluminum layered double hydroxide (CuAl-LDH); hyaluronic acid (HA) pH-responsive; CD44-targeting property of HA LDH/HA/5-FU nanosheets could rapidly release Cu (II) and 5-FU in tumor cells, and induce tumor cell apoptosis and cuproptosis. LDH/HA/5-FU nanosheets show excellent inhibitory effects on tumors by combining Cu-based chemical dynamics therapy (CDT) and chemotherapy [ 208 ] PTC Cu 2 O, AIE photosensitizer (TBP-2), Platelet vesicle (PV), Acid conditions and hydrogen peroxides; light irradiation PTC therapy can specifically induce cuproptosis in tumor cells, significantly suppressing the lung metastasis of breast cancer, increasing the population of central memory T cells in peripheral blood, and preventing tumor recurrence [ 211 ] Au@MSN-Cu/PEG/DSF Au nanorods (NRs), Cu(NO 3 ) 2 , PEG, DSF PTT Au@MSN Cu/PEG/DSF can effectively induce tumor cell death and suppress tumor growth in synergy with PTT [ 212 ] O 2 -PFH@CHPI NPs Cu 2+ ; indocyanine green; O 2 -saturated perfluorohexane (PFH) pH-Responsive; PTT Upon NIR...…”

Thiosemicarbazone Mixed-Valence Cu(I/II) Complex against Lung Adenocarcinoma Cells through Multiple Pathways Involving Cuproptosis

“…Interestingly, complex 2 damages cells by triggering multiple mechanisms that involve cuproptosis. The mechanism of action of cuproptosis is different from the modes of cell death that have been extensively studied, such as apoptosis and necrosis, and as such, it shows great promise in overcoming the shortcomings of current tumor therapies. , Currently, cuproptosis is mainly executed by organic small-molecule copper ionophores (such as elesclomol) binding to copper in cells , or by delivering exogenous copper ions to cells via nanoplatforms. ,− Even although the concentration of Cu in many human tumor tissues is higher than in normal tissues, the concentration of copper in tumor tissues is still too low, which can lead to a potentially suboptimal effect of cuproptosis induced by organic small-molecule copper ionophores . The construction of nanoplatforms often requires complex operations.…”