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. 2019 Jul 26;19:256–266. doi: 10.1016/j.isci.2019.07.036

Figure 6.

Figure 6

GGCT in Cellular Stress Alleviation

(A, B) Cellular ROS level was quantified by carboxy-H2DCFDA flow cytometry in primary wild-type and GGCT−/− MEFs; error bars represent mean ± SD of four experiments.

(C) GSH level was quantified by mass spectrometry in primary wild-type and GGCT−/− MEFs; error bars represent mean ± SD of three experiments.

(D) L-cysteine level was quantified by mass spectrometry in primary wild-type and GGCT−/− MEFs; error bars represent mean ± SD of three experiments.

(E) The proliferation defect of GGCT−/− MEFs can be rescued by ROS scavenger N-acetylcysteine (NAC, 1 mM) treatment. Error bars represent mean ± SD of three experiments.

(F) Proposed model for GGCT function in cancer. Both oncogenic signal (like RAS activation) and chromosomal 7p14.3 locus amplification lead to GGCT expression up-regulation in human cancers. GGCT helps to alleviate oncogenic stress by regulating GSH-ROS metabolism. In the absence of GGCT, the accumulated cellular stress leads to cell proliferation arrest and cell senescence. For all comparisons, p values of unpaired two-tailed t test are shown.