Fig. 7: G6PD and H3R17me2 are upregulated in gastric cancer. | Cell Death & Disease

Fig. 7: G6PD and H3R17me2 are upregulated in gastric cancer.

From: The NRF2-CARM1 axis links glucose sensing to transcriptional and epigenetic regulation of the pentose phosphate pathway in gastric cancer

Fig. 7

A Representative IHC images of G6PD, H3R17me2, and Ki67 levels in specimens from 8 patients with stomach adenocarcinoma (T) and matched adjacent noncancerous (N) tissues. Brown staining indicates the expression of the indicated target protein. Scale bars, 200 μm. B G6PD and H3R17me2 protein expression levels based on the staining index in gastric adenocarcinoma samples (n = 8) and normal adjacent tissues (n = 8). C, D Western blot analysis of G6PD and H3R17me2 in gastric cancer tissues and matched adjacent noncancerous tissues. β-actin and histone H3 were used as loading controls in all immunoblots. E Working model for the NRF2-CARM1 axis enhancing the viability and proliferation of gastric cancer cells in glucose-deficient conditions by modulating the PPP. Glc represents glucose. All data are shown as mean ± SEM. P values were determined by two-tailed t-tests. Values of P < 0.05 were considered statistically significant. *P < 0.05, **P < 0.01, and ***P < 0.001.

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