Fig. 6: TCP1 promotes the development of HCC and regulates the AKT/GSK-3β and ERK signalling pathways in a DEN-induced mouse model. | Communications Biology

Fig. 6: TCP1 promotes the development of HCC and regulates the AKT/GSK-3β and ERK signalling pathways in a DEN-induced mouse model.

From: TCP1 promotes the progression of malignant tumours by stabilizing c-Myc through the AKT/GSK-3β and ERK signalling pathways

Fig. 6

a Establishment scheme for wild-type and TCP1-ROSA26 knock-in mice and diagram of the DEN-induced mouse primary HCC model. b, c The numbers of tumour nodules (red arrows), the liver weight ratios, and tumour volumes of the WT and TCP1-KI mice were calculated and analysed. Images of hepatomas (b) the liver/body weight ratio, the tumour number, and the tumour volume are shown (c). d The relationship between the number of tumour nodules and tumour volume. e, g HE staining and IHC were carried out to observe the structure of liver tissues and assay the levels of AFP, TCP1, c-Myc, and Ki67 in the WT and TCP1-KI mouse models. Scale bar, 200 μm. f, h c-Myc, p-c-MycT58, p-c-MycS62, AKT, p-AKTS473, GSK-3β, p-GSK-3βS9, p-ERK, and ERK were detected in WT and TCP1-KI mouse tissues to determine the effect of overexpressing TCP1 in vivo. The data are shown as the means ± SD from three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, between the indicated groups.

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