Figure 8: Dex represses H22 hepatocarcinoma.

(a) Dex inhibited the growth of ectopic hepatocarcinoma. BALB/c mice were inoculated with H22 cells into the right flank and treated with 0, 1.25, 2.5 or 5 μg g⁻¹ Dex. The growth of tumour was monitored (n=6, each group). (b) BALB/c mice were inoculated with H22 cells and treated with 0 or 2.5 μg g⁻¹ Dex on day 4, once per day for 7 days. On day 11, Dex treatment was withdrawn in half of the treated mice and the remaining mice were continued with 2.5 μg g⁻¹ Dex treatment. The growth of tumour was monitored (n=6, each group). (c,d) Dex inhibited the growth of orthotopic hepatocarcinoma. BALB/c mice liver were inoculated with H22 cells and treated with 0, 1.25, 2.5 or 5 μg g⁻¹ Dex. The typical size of tumours (c) and tumour weight (d) on day 16 were shown (n=5, each group). (e) Dex did not affect the growth of B16 melanoma. C57BL/6 mice were inoculated with B16 cells into the right flank and treated with 0, 1.25, 2.5 and 5 μg g⁻¹ Dex. The growth of tumour was monitored (n=6, each group). (f) Knockdown of PEPCK promoted the formation of H22 tumour ascites. H22 tumour cells (1 × 10⁵) were i.p. injected to mice. Two days later, mice were treated with 2.5 μg g⁻¹ Dex. At the same time, the chemically modified 2′-O-methyl, 5′-cholesterol siRNA for PEPCK and scrambled siRNA (10 nmol in 0.2 ml saline buffer, each) were also i.p. injected to the mice once per 3 days. Ten days later, mice were killed and the ascites were measured (n=6, each group). *P<0.001. In the box and whisker plots, the box contains 50% of the data. Twenty five per cent of the data are greater than the top of the box and 25% of the data are less than the bottom of the box. The line in the box represents the median. (g) 3-MPA impaired the inhibitory effect of Dex on H22 hepatocarcinoma. BALB/c mice were inoculated with H22 cells into the right flank and treated with 2.5 μg g⁻¹ Dex or 2.5 μg g⁻¹ Dex+30 μg g⁻¹ 3-MPA. The growth of tumours was monitored (n=6, each group). (h,i) Prednisone does not influence the expression of PEPCK and G6Pase and tumour growth. H22 tumour cells were treated with 0, 0.1, 1 and 10 μM prednisone for 7 days. The expression of PEPCK and G6Pase was analysed by reverse transcriptase–PCR (h). Mice were inoculated with H22 cells and treated with 0, 1.25, 2.5 or 5 μg g⁻¹ prednisone. The tumour growth was monitored (i). Data shown are representative of three independent experiments and error bars represent means±s.e.m., *P<0.05, **P<0.01 (analysis of variance (ANOVA)).