Fig. 5: TXNIP is responsible for DSF-induced mitochondrial dysfunction. | Cell Death & Disease

Fig. 5: TXNIP is responsible for DSF-induced mitochondrial dysfunction.

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

Fig. 5

A Significantly changed genes by RNA-seq comparing vemurafenib-resistant cells treated with Vem+DSF to cells treated with Vem. B WB of TXNIP expression in vemurafenib-resistant cells exposed to Vem or Vem+DSF. C CCK-8 assay of vemurafenib-resistant cells with TXNIP knockout exposed to Vem+DSF or Vem. D Colony formation of vemurafenib-resistant cells with TXNIP knockout exposed to Vem+DSF or Vem. E TEM observation of vemurafenib-resistant cells with TXNIP knockout exposed to Vem+DSF or Vem. F Immunofluorescence staining of MMP levels in vemurafenib-resistant cells with TXNIP knockout exposed to Vem+DSF or Vem. G ATP content in vemurafenib-resistant cells with TXNIP knockout exposed to Vem+DSF or Vem. H Seahorse assay of vemurafenib-resistant cells with TXNIP knockout exposed to Vem+DSF or Vem. I Flow cytometry assay of mt-ROS levels in vemurafenib-resistant cells with TXNIP knockout exposed to Vem+DSF or Vem. J–L Tumors removed from nude mice bearing 451Lu-R ko-NC cells or 451Lu-R ko-TXNIP after 14 days of treatment with Vem+DSF or Vem (J). Tumor volumes and weights in each group were calculated and displayed in (K) and (L). Symbols of one dot indicate one mouse, and the error bars are mean ± SD. The differences were analyzed using Student’s t-test and one-way ANOVA. *P < 0.05, **P < 0.01, and ***P < 0.001. ns non-significant, ko-NC knockout negative control, ko-TXNIP knockout of TXNIP.

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