Fig. 1: TRIM25 functions as a feedback mechanism that responds to ER stress in tumor cells. | Nature Communications

Fig. 1: TRIM25 functions as a feedback mechanism that responds to ER stress in tumor cells.

From: TRIM25 promotes the cell survival and growth of hepatocellular carcinoma through targeting Keap1-Nrf2 pathway

Fig. 1

a Relative mRNA fold change of all TRIMs in HCT116 cells treated with TM (Tunicamycin, 5 μg/ml) or TG (Thapsigargin, 1 μM) for 6 h. b Western blot analysis the level of TRIM25 and GRP78 in HCT116 and Huh7 cells treated with TM (5 μg/ml) or TG (1 μM) for 12 h. c Relative mRNA fold change of TRIM25 and BiP genes in HCT116 and Huh7 cells after stable knockdown of TRIM25. d Relative mRNA fold change of UPR genes: sXBP1, ATF4, CHOP in HCT116 cells with control (shNC) or stable knockdown of TRIM25. e Relative mRNA fold change of UPR genes: sXBP1, ATF4, CHOP in HCT116 cells stably overexpressing control or F-TRIM25 (Flag-TRIM25), treated with or without TG (1 μM) for 6 h. f Western blot analysis of UPR signaling, including phospho-JNK/JNK and phospho-eIF2α/eIF2α in HCT116 cells after stable knockdown of TRIM25 in HCT116 cells. g Western blot analysis of the levels of phospho-JNK/JNK andphospho-eIF2α/eIF2α in HCT116 cells overexpressing control or F-TRIM25, treated with or without TG (1 μM) for 12 h. h, i Western blot analysis of the levels of phospho-JNK/JNK in Huh7 cells after stable knockdown (h) or overexpression (i) of TRIM25, treated with or without TG (1 μM) for 12 h. For c–e, data represent the mean ± SEM (n = 3). Statistical significance was assessed using two-tailed Student’s t-tests.

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