Fig. 3: AD treatment augments the proteasomal degradation of PTPMT1 in HCC cells. | Cell Death & Disease

Fig. 3: AD treatment augments the proteasomal degradation of PTPMT1 in HCC cells.

From: Pharmacological targeting of the mitochondrial phosphatase PTPMT1 sensitizes hepatocellular carcinoma to ferroptosis

Fig. 3

Hep 3B cells underwent treatment with AD at concentrations of 0, 0.5, 1, and 2 μM for a duration of 24 h, after which they were collected for PTPMT1 assay (A). Separately, cells exposed to 1 μM AD were harvested at distinct time intervals (0, 4, 8, 12, 16, and 24 h), and the protein expression of PTPMT1 and FTL was analyzed via western blotting (B). Data are depicted as mean ± SD. A P value below 0.05 was deemed statistically significant. *: P < 0.05 relative to the Ctrl group. To ascertain the half-life of PTPMT1, HCC cells were treated with cycloheximide to inhibit protein synthesis, and PTPMT1 expression was assessed at various time points through western blotting (C). The intensity of the PTPMT1 band, normalized to TUBULIN, against time is illustrated in the subsequent plot (D). In this study, a PTPMT1 knockout cell line was established using the CRISPR/Cas9 system, with the knockout efficacy verified via immunoblotting (E). Furthermore, both wild type (WT) and PTPMT1 knockout (KO) cells were subjected to AD treatment, and the susceptibility of AD (1 μM)-treated cells to Erastin (10 μM)-induced ferroptosis (24 h) was assessed through cell viability assays (F) and BODIPY staining (G). *:P < 0.05 compared between the two groups.

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