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. Author manuscript; available in PMC: 2011 Jan 22.
Published in final edited form as: Cell. 2010 Jan 22;140(2):197–208. doi: 10.1016/j.cell.2009.12.052

Figure 4. Obese HCC-bearing mice exhibit activated STAT3 and elevated expression of inflammatory cytokines.

Figure 4

The HCC-bearing mice from Figure 2 were subjected to additional biochemical and gene expression analyses.

(A). Activation state of metabolically-regulated protein kinases. Non-tumor (NT) liver and HCC (T) were lysed, gel separated and the activation (phosphorylation) states of AKT and S6 kinase (S6K) were examined by immunoblotting.

(B). Non-tumor (NT) liver and HCC (T) were analyzed for phosphorylation of JNK, ERK, p38, and STAT3 by immunoblotting as above. The bottom panel shows JNK kinase assays in non-tumor liver and HCCs of 4 different mice per dietary group.

(C). The results of several immunoblots similar to the one shown in B, each representing a different mouse, were quantitated using Image J software and mean values were determined (n=3-4).

(D). Serum IL-6 in HCC-bearing mice was determined by ELISA (n=10-12).

(E-G). Relative amounts of IL-6 (E), TNF (F) and IL-1β (G) mRNAs in non-tumor (NT) liver and HCC (T) were determined by qRT-PCR and normalized to cyclophilin mRNA (n=6-8).

(H). TNF amounts in non-tumor liver (NT) and HCC (T) were examined by immunoblotting of tissue lysates.

All values represent means ± s.d. *P<0.05, **P<0.01, ***P<0.001 denote significant differences between the groups. See also Supplemental Figure S3.