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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Novel Pt@PCN-Cu-induced cuproptosis amplifies αPD-L1 immunotherapy in pancreatic ductal adenocarcinoma through mitochondrial HK2-mediated PD-L1 upregulation

Fig. 3

Pt@PCN-Cu induces robust intracellular ROS generation and severe mitochondrial damage, triggering cuproptosis. (A) CLSM images of PANC-1 cells stained with JC-1, illustrating changes in mitochondrial membrane potential following various treatments. Scale bar: 10 μm. (B) Representative CLSM images showing intracellular ROS generation in PANC-1 cells treated with different treatments. Scale bar: 100 μm. (C) TEM images of PANC-1 cells, highlighting mitochondrial morphology after PBS or Pt@PCN-Cu treatment. Scale bar: 500 nm. (D) Western blot analysis of DLAT, LIAS and FDX1 expression levels in PANC-1 cells after various treatment. (E) DLAT expression levels in PDAC tissues and normal pancreatic tissues analyzed using GEPIA2 (http://gepia2.cancer-pku.cn/). (F) Correlation between DLAT expression and OS and DFS in PDAC patients, as evaluated through GEPIA2. (G) Positive correlations between DLAT expression and the expression of LIAS in PDAC tumor tissues using GEPIA2. (H) LDH release assay quantifying membrane damage in PANC-1 cells subjected to the indicated treatments. (I) Measurement of intracellular ATP levels in PANC-1 cells after different treatments. (J) Measurement of intracellular GSH levels after various treatments. (K) Glucose consumption measured using a glucose assay kit. (L) Lactate production assessed using a lactate production detection kit. Data are presented as mean ± SD. Statistical analysis was performed using t-test or one-way ANOVA, with *P < 0.05, **P < 0.01 and ***P < 0.001

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