Fig. 3: The levels of PGAM5 affected cells chemosensitivity and 5-Fu induced apoptosis in HCC cells. | Cell Death & Disease

Fig. 3: The levels of PGAM5 affected cells chemosensitivity and 5-Fu induced apoptosis in HCC cells.

From: High PGAM5 expression induces chemoresistance by enhancing Bcl-xL-mediated anti-apoptotic signaling and predicts poor prognosis in hepatocellular carcinoma patients

Fig. 3

a Silence of PGAM5 inhibited HCC cell viability, whereas replenishment of PGAM5 rescued the cell viability inhibition after treatment with 5-Fu for 48 h at indicated dose. Cell viability was examined by CCK-8 assay. Data represent the mean ± SD from three individual experiments with triplicate wells (*p < 0.05; **p < 0.01, Student’s t-test). shRNA#2 had a better effect and was chosen for further study. b Silencing of PGAM5 sensitizes cells to 5-Fu induced apoptosis, whereas the apoptotic rate was attenuated after re-overexpression of PGAM5. Cell apoptotic death events were monitored by Annexin V/PI staining and flow cytometry assays. The percentage of cell apoptosis was shown as the mean ± SD from three independent experiments (*p < 0.05; **p < 0.01,Student’s t-test). c Cleaved caspase 3 and PARP induced by 5-Fu treatment were determined by Western blotting, and β-actin was used as a normalized control

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