Verteporfin reversed these effects...MMRN1 acts as a tumor suppressor in TC by activating the Hippo pathway and modulating oxidative stress and ferroptosis. These findings highlight MMRN1 as a potential therapeutic target for TC treatment.

COX17 may enhance copper accumulation, oxidative stress, tumor-cell-death-associated changes, and angiogenesis-related phenotypic inhibition. Further studies using canonical cuproptosis markers, copper chelator rescue experiments, additional gastric cancer cell lines with different p53 backgrounds, and clinical validation are required to confirm the translational significance of this pathway.

Here, we demonstrate that elesclomol-induced cuproptosis potently activates innate and adaptive antitumor immunity, markedly enhancing CD8+ T cell cytotoxicity while attenuating exhaustion...We further show that FDX1 binds DICER1 to reduce DMBT1 mRNA stability, with FDX1 and DMBT1 expression exhibiting significant negative correlation in CRC tissues. Our findings establish the FDX1-DICER1-DMBT1 axis as a critical regulator of CRC progression and immune evasion, suggesting that therapeutic targeting of this pathway could enhance antitumor immunity and overcome resistance to existing immunotherapies.

Bel-sar (belzupacap sarotalocan) is a first-in-class virus-like drug conjugate composed of a tumor-targeting virus-like particle linked to a photoactivatable dye, inducing proimmunogenic tumor cell death and antitumor immune response...Bel-sar demonstrated focal administration feasibility, a favorable safety profile, and encouraging preliminary efficacy in NMIBC, with robust immune activation in treated and untreated tumors. These findings support bel-sar's continued development as a therapy combining local tumor eradication with durable immune surveillance.

P2, N=24, Active, not recruiting, Mayo Clinic | Trial completion date: Dec 2029 --> Mar 2031 | Trial primary completion date: Dec 2029 --> Mar 2028 | Recruiting --> Active, not recruiting

Increased NDUFB3 expression in RANBP1-overexpressing cells was reversed by YAP1 inhibitor verteporfin treatment or knocking down YAP1. RANBP1 enhances a more invasive microenvironment of OSCC.

Dendritic SiO2 nanoparticles were sequentially loaded with elesclomol-copper complex (ESCu) and hemin, followed by hyaluronic acid (HA) coating to achieve CD44-mediated tumor targeting and HAase/pH-responsive drug release...In vivo results further demonstrated enhanced tumor accumulation, superior tumor growth inhibition, and favorable preliminary biosafety. This work provides a targeted nanotherapeutic strategy for enhanced cancer treatment through cuproptosis-photothermal combination therapy.

Notably, combining the SIRT5 inhibitor MC3482 with the cuproptosis inducer Elesclomol-Cu synergistically suppresses tumor growth in vivo, suggesting a promising therapeutic strategy. These findings elucidate mechanisms underlying cuproptosis resistance and propose a novel treatment approach for LUAD.

Elesclomol (15 nM) and copper chloride (CuCl₂, 10 µM) were used to induce cuproptosis, while DLAT overexpression and S6 kinase inhibition were used to clarify signaling processes. MELK expression was considerably elevated in DLBCL tissues and cell lines (P < 0.05)...On the other hand, MELK-mediated effects on cuproptosis and intracellular copper buildup were abolished by S6K suppression or DLAT overexpression. Through the PI3K/mTOR/S6K-DLAT axis, MELK imparts resistance to cuproptosis and increases DLBCL cell survival. MELK targeting may increase copper-induced cytotoxicity, offering a possible DLBCL treatment approach.

Herein, a carrier-free GSH-responsive in situ nanoreactor (TECJ) is fabricated, of which Cu ionophore elesclomol (ES), GSH-responsive nitric oxide (NO) donor O2-(2,4-dinitrophenyl) 1-[(4-ethoxycarbonyl) piperazin-1-yl] diazen-1-ium-1,2-diolate (JSK) and Cu2+ are integrated via self-assembly and coated with D-α-tocopherol polyethylene glycol 1000 succinate (TPGS)...Afterwards, the process above synergistically activates immunogenic cell death and cascades immunotherapy. Finally, TECJ successfully suppresses tumor growth and prevents tumor metastasis.

In patient-derived models, high HSF2/FDX1 expression predicts enhanced response to cuproptosis inducers. Our work establishes an epigenetic mechanism linking copper sensing to cuproptosis and nominates the CHD4/HSF2/FDX1 axis as potential biomarkers and therapeutic targets for precision oncology.

Furthermore, the cuproptosis activator elesclomol, inhibitor TTM, and Ras activator ML-098 were used...In vivo, 10 mg/kg Licochalcone A reduced tumor volume/weight by 42.27 ± 11.63%/45.13 ± 13.15%, with consistent protein changes (FDX1, LIAS, RAS, p-MEK and p-ERK). Collectively, it induces glioma cuproptosis via inactivating RAS/ERK, providing a potential therapeutic target.