Fig. 1: DSF inhibits BRAFi-resistant melanoma growth in a copper-dependent way. | Cell Death & Disease

Fig. 1: DSF inhibits BRAFi-resistant melanoma growth in a copper-dependent way.

From: Exploiting mitochondrial dysfunction to overcome BRAF inhibitor resistance in advanced melanoma: the role of disulfiram as a copper ionophore

Fig. 1: DSF inhibits BRAFi-resistant melanoma growth in a copper-dependent way.The alternative text for this image may have been generated using AI.

A CCK-8 assay of cell viability of two vemurafenib-resistant cell lines treated with vemurafenib (Vem) alone, disulfiram (DSF) alone, or Vem in combination with DSF for 48 h. B–D Images of tumors from mice that received Vem alone, DSF alone, or Vem in combination with DSF (B). Tumor volumes and weights in each group were measured and displayed in (C) and (D). E Viability of vemurafenib-resistant cells with and without pretreatment of 20 μM TTM exposed to Vem or Vem+DSF. F Viability of vemurafenib-resistant cells pretreated with 30 μM Z-VAD-FMK (ZVF) and 50 μM D-Boc-FMK(DBF), followed by treatment with Vem or DSF+Vem. G Viability of vemurafenib-resistant cells pretreated with 20 μM Necrostatin-1 (NEC-1), followed by treatment with Vem or DSF+Vem. H Viability of vemurafenib-resistant cells pretreated with 10 μM ferrostatin-1 (FER-1), followed by treatment with Vem or DSF+Vem. I Viability of vemurafenib-resistant cells pretreated with 5 μM chloroquine (CQ), followed by treatment with Vem or DSF+Vem. J–L Images of tumors from mice that received the indicated treatment (J). Tumor volumes and weights in each group were measured and displayed in (K) and (L). The symbol of one dot indicates one tumor sample, and the error bars are the mean ± SD. The differences were analyzed using one-way ANOVA. *P < 0.05, **P < 0.01, and ***P < 0.001. ns non-significant, ZVF Z-VAD-FMK, BDF Boc-D-FMK, NEC-1 Necrostatin-1, FER-1 Ferrostatin-1, CQ chloroquine.

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