Table 2 The anti-breast cancer effect of copper ionophores
From: Cuproptosis: a promising new target for breast cancer therapy
Compound | Cancer type | Materials (cell lines) | Combined drugs | Anti-tumor efect and its involved mechanism | Refs. |
|---|---|---|---|---|---|
Elesclomo | Breast cancer | MCF-7, MDA-MB-231, HCC1806 | DOX, paclitaxel | Elesclomol moderately curbs breast cancer cell growth and boosts DOX/paclitaxel-induced apoptosis, partly through the JNK1 pathway | [107] |
Elesclomol | Breast cancer | BRCA1-mutated breast cancers cells, Basal-like breast cancers cells | Â | BRCA1-mutated and/or basal-like breast cancer cells sensitive to elesclomol due to defective oxidative DNA repair | [108] |
Disulfram | Breast cancer | MCF-7, SKB-R3, MDA-MB-435Â S | Cisplatin | Disulfram curbs ALDH, reduces breast cancer stemness, and boosts cisplatin toxicity | [104] |
Disulfram | Breast cancer | MCF-7, MDA-MB-231 |  | Disulfram blocks TGF-β-induced EMT in breast cancer via ERK/NF-κB/Snail downregulation | [102] |
Disulfram | Breast cancer | LLC, B16 | Â | Disulfram halts FROUNT-chemokine interaction, inhibiting macrophages and reducing tumor progression | [109] |
Disulfram | Breast cancer | BT-549, MDA-MB-231 | Â | Disulfram boosts anti-PD-1 therapy in TNBC by epigenetic IRF7 reactivation, modulating PD-L1 | [110] |
Disulfram | Breast cancer | MCF-7 | DOX, hydrazine | The triple therapy of DOX, disulfram, hydrazine boosts chemosensitivity by synergistically reducing DOX dose for eradicating resistant MCF-7 cells | [111] |
Disulfram/Cu | Breast cancer | MCF-7, MDA-MB-231 | Â | CuET inhibits NPL4/p97-mediated protein degradation, suppressing tumor growth | [103] |
Disulfram/Cu | Breast cancer | MCF7, MDA-MB-231, T47D | Paclitaxel | Disulfram–Cu halts breast cancer stem cell growth, boosts paclitaxel cytotoxicity in breast cancer cells, likely via ROS induction and NF-κB inhibition | [101] |
Disulfram/Cu | TNBC | MDA-MB-231PAC10 | Paclitaxel/cisplatin | Disulfram–Cu inhibits the expression of cancer stem cell markers and reverses paclitaxel and cisplatin resistance in MDA-MB-231PAC10 cells | [105] |
Disulfram/Cu | Breast cancer | MDA-MB-231, MCF10DCIS.com |  | Disulfram–Cu induces apoptosis and suppresses breast cancer xenograft growth by inhibiting proteasome activity | [12] |
Disulfram/Cu | Breast cancer | MDA-MB-231, BT20, MDA-MB-231PIK3CA H1047R, MDA-MB-231PIK3CA-E545K |  | Disulfram–Cu decreases PTEN expression and AKT activation in breast cancer cells, and when combined with the PI3K inhibitor LY294002, it potently suppresses the growth of xenografts formed by MDA-MB-231 cells harboring mutant PIK3CA-H1047R or PIK3CA-E545K | [112] |
Disulfram/Cu | TNBC | MDA-MB-231, 4T1 |  | Disulfram–Cu treatment triggers apoptosis in TNBC cells through caspase-3 activation and selectively targets cancer stem cell-like populations, with these effects attributed to significant disruption of the STAT3 signaling pathway | [113] |
Disulfram/Cu | Breast cancer | BT474, SKBR3 |  | Disulfram–Cu triggers apoptosis and eliminates cancer stem-like cells in HER2-positive breast cancer by inhibiting the HER2/Akt signaling pathway | [114] |
Disulfram/cadmium (Cd) Breast cancer | Breast cancer | MCF10DCIS, MCF10A |  | Disulfram–Cd selectively disrupts proteasome function and induces apoptosis in human breast cancer cells, while leaving non-tumorigenic cells unaffected | [115] |
Disulfram/Cu | Breast cancer | MDA-MB-231, Hs578T |  | Disulfram–Cu exhibits anti-migratory and anti-invasive effects by inducing focal adhesion loss and cytoskeletal collapse, thereby inhibiting tumor growth and lung colonization in triple-negative breast cancer (TNBC) | [116] |
Disulfram/Cu | Breast cancer | MCF-7, HT-29 |  | An acidic pH significantly augments the toxicity of the disulfram–Cu complex in breast and colon cancer cells. This effect is correlated with alterations in cell metabolism, modulation of Akt kinase and NF-κB activity, and elevated production of reactive oxygen species (ROS) | [117] |