Fig. 3: ML-323 induces hepatocarcinoma cancer (HCC) cell apoptosis via the ATF4-Noxa axis. | Cell Death & Disease

Fig. 3: ML-323 induces hepatocarcinoma cancer (HCC) cell apoptosis via the ATF4-Noxa axis.

From: Inhibition of USP1 activates ER stress through Ubi-protein aggregation to induce autophagy and apoptosis in HCC

Fig. 3

A Annexin V-FITC /PI double-staining showing apoptotic Noxa-deficient HCC cells treated with ML-323. HCCLM3 and SMMC-7721 cells were transfected with control siRNA or Noxa siRNA and then treated with ML-323 for 48 h. B Western blot analysis showing the efficiency of siNoxa and its effects on cleaved-PARP levels. HCCLM3 and SMMC-7721 cells were treated as shown in (A). C Western blot analysis of Noxa-related transcription factors. HCCLM3 and SMMC-7721 cells were treated with DMSO or ML-323, and cell lysates were analyzed by western blotting using specific antibodies. D Annexin V-FITC /PI double-staining of ATF4-deficient HCC cells treated with ML-323. After transfection with control or ATF4 siRNA, HCCLM3 and SMMC-7721 cells were treated with ML-323 for 48 h. E Western blot analysis of the knockdown efficiency of siATF4 and its effect on the expression of Noxa and cleaved-PARP. F Western blot analysis of ubiquitinated proteins and ER stress-related proteins. HCCLM3 and SMMC-7721 cells were treated with ML-323. All the data represent at least three independent experiments (n = 3; error bars, SD). All data represented at least three independent experiments (n = 3; Error bars, SD).

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