Figure 2: Abnormal expression of 11β-HSD1 and 11β-HSD2 in mouse hepatocarcinoma. | Nature Communications

Figure 2: Abnormal expression of 11β-HSD1 and 11β-HSD2 in mouse hepatocarcinoma.

From: Switch of glycolysis to gluconeogenesis by dexamethasone for treatment of hepatocarcinoma

Figure 2

(a) The expression of GR in hepatocarcinoma and normal liver tissue was detected by reverse transcriptase–PCR (upper) and western blot (bottom). (b) The expression of 11β-HSD1 and 11β-HSD2 in H22 hepatocarcinoma was analysed by reverse transcriptase–PCR (RT–PCR; left) and real-time PCR (right). (c) Immunohistochemical analysis of 11β-HSD1 and 11β-HSD2 in H22 hepatocarcinoma tissue. Scale bar, 20 μm. (d) The expression of 11β-HSD1 and 11β-HSD2 in H22 tumour cells was analysed by RT–PCR (left) and real-time PCR (right). (e) Upregulation of PEPCK and G6Pase by 11β-HSD1 overexpression and 11β-HSD2 knockdown. H22 cell line with 11β-HSD1 overexpression or 11β-HSD2 knockdown was injected to mice. The expression of PEPCK and G6Pase in hepatocarcinoma tissues was detected by RT–PCR (left) and real-time PCR (right). Data shown are representative of three independent experiments and error bars represent means±s.e.m., *P<0.05, ** P<0.01, *** P<0.001 (analysis of variance).

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