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Fig. 5 | Journal of Experimental & Clinical Cancer Research

Fig. 5

From: Loss of Ufl1/Ufbp1 in hepatocytes promotes liver pathological damage and carcinogenesis through activating mTOR signaling

Fig. 5

Hepatic Ufl1 or Ufbp1 deficiency results in spontaneous liver carcinomas in 14-month old mice. A Anatomic illustration of liver tissues extracted from 14-month-old Ufl1Δ/Δhep, Ufbp1Δ/Δhep, and control mice. B Histological analysis of liver tissues extracted from 14-month-old Ufl1Δ/Δhep, Ufbp1Δ/Δhep, and control mice by H&E staining. Arrow: foam cells/macrophages/apoptotic cells. C Immunostaining of the liver tumor marker AFP and the proliferation marker Ki67 in liver tissues extracted from 14-month-old Ufl1Δ/Δhep and control mice. Quantitative data are shown in the right panel (n = 5 mice/group). D Western blot analysis of the key molecules involved in mTOR signaling from samples extracted from 14-month-old Ufl1Δ/Δhep, Ufbp1Δ/Δhep, and control mice. All western blots were independently repeated at least three times with consistent results. Quantitative data are shown in the right panel. E Immunostaining of GβL in liver tissues extracted from 14-month-old Ufbp1.Δ/Δhep and control mice. Quantitative data are shown in the right panel (n = 5 mice/group). Immunofluorescence showing colocalization of Ufl1 and mTOR F or Ufbp1 and mTOR G in 14-month-old mice. Quantitative data are shown in the right panel (n = 5 mice/group). ** p < 0.01; *** p < 0.001

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