Fig. 2: ER stress stimulates GOLGA2P10 transcription via the PERK/ATF4/CHOP signaling pathway.

a Treatment with actinomycin D abrogated tunicamycin-induced GOLGA2P10 expression. MHCC-97H cells treated with DMSO or tunicamycin were incubated without or with actinomycin D (actD) for 13 h before qPCR analysis. b, c Silencing of PERK or ATF4 diminished tunicamycin-induced GOLGA2P10 expression in MHCC-97H cells. d, e CHOP knockdown abrogated tunicamycin- and thapsigargin-induced GOLGA2P10 expression. For b–e, hepatoma cells were reversely transfected with the indicated RNA duplexes for 36 h, then cultured with DMSO (b–e), tunicamycin (b–d), or thapsigargin (e) for an additional 16 h before qPCR analysis. iMAX, cells exposed to Lipofectamine RNAiMAX but not RNA duplexes. NC, negative control for siRNAs. For a–e, data are shown as mean ± SEM of three independent experiments. f CHOP was upregulated in HCC tissues. The mRNA level of CHOP was detected in 31 paired HCC (T) and adjacent non-tumor liver tissues (N) by qPCR analysis. The mean value of adjacent non-tumor liver tissues was set as relative level 1. g HCCs with CHOP elevation displayed higher GOLGA2P10 expression. The levels of CHOP or GOLGA2P10 in HCC tissue relative to that in adjacent non-tumor tissue (T/N), based on data from Figs. 2f and 1c, were used for analysis. T/N = 1.5 was chosen as the cut-off point for separating the tumors without (−) CHOP-upregulation (n = 19) from those with (+) CHOP-upregulation (n = 12). β-actin was used as an internal control. *P < 0.05; **P < 0.01; ***P < 0.001; ns not significant.