Fig. 2: The impact of PGAM5 on HCC cell proliferation and apoptosis. | Cell Death & Disease

Fig. 2: The impact of PGAM5 on HCC cell proliferation and apoptosis.

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

Fig. 2

a The levels of PGAM5 protein in 5 HCC cell lines, the immortalized liver cell line LO2 and 3 non-neoplastic hepatic tissues were examined by western blotting. b Cell viability of 5 HCC cell lines to 5-fliorouracil (5-Fu) were examined by CCK-8 assay. c Two PGAM5 shRNA (shRNA#1 and shRNA#2) were introduced to two HCC cell lines (7402 and HepG2), for stable knockdown of PGAM5 through recombinant lentiviral infection. Then, pCDH-PGAM5 lentiviral particles were transduced into above PGAM5-silened HCC cells to replenish PGAM5 expression. The levels of PGAM5 were examined by western blotting. Control = non-silencing scramble RNA sequence control; shRNA and shPGAM5 = shRNA targeting PGAM5 mRNA; PGAM5 = PGAM5-silened HCC cells with restoring the expression of PGAM5. d, e Silence of PGAM5 inhibits the proliferation of 7402 (d) and HepG2 (e) cells. The cell viabilities were detected by CCK-8 assay (*p < 0.05; **p < 0.01; Student’s t-test). f Depletion of PGAM5 increased the apoptotic rate in HCC cells. Apoptotic cells were monitored by Annexin V/propidium iodide staining and flow cytometry assays. Data represent mean values and S.E (*p < 0.05; Student’s t-test). All Data represent the mean ± S.E derived from three indivicual experiments with triplicate wells. Error bars, S.E

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