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Fig. 2 | Journal of Experimental & Clinical Cancer Research

Fig. 2

From: HMGA1-TRIP13 axis promotes stemness and epithelial mesenchymal transition of perihilar cholangiocarcinoma in a positive feedback loop dependent on c-Myc

Fig. 2

HMGA1 promoted the transcription and expression of TRIP13. a Heatmap and hierarchical clustering analysis revealed 180 up-regulated gene expression profiles in eight pairs of pCCA tissues and adjacent normal tissues. TRIP13 was filtered out as the only overlapping gene between the 21 Proteomic HMGA1-linked signature and 180 total upregulated genes (a). c Correlations between HMGA1 and LRRC59/KIFC1/TRIP13 mRNA in 36 cases of CCA were evaluated. The linear correlations were analyzed using the Spearman method. d Changes in LRRC59/KIFC1/TRIP13 mRNA after knocking down or overexpressing HMGB1 in QBC939 cells. e Correlation between HMGA1 and TRIP13 mRNA in 12 fresh pCCA tissues. mRNA ratio was calculated by mRNA (tumor)/mRNA (adjacent tissue). f Representative IHC images of low and high TRIP13 expression (top: 100× magnification, scale bar, 200 μm; bottom: 400× magnification, scale bar, 50 μm). g IHC scores of HMGA1 were significantly associated with TRIP13 scores in pCCA tissues. h Patients with high HMGA1 expression had higher TRIP13 expression. i TRIP13 expression was detected in stable QBC939 cells with HMGA1 knockdown or overexpression. j and k HMGA1 promoted the transcription of TRIP13 in both QBC939 and FRH0201 cells (j), and 293 T cells(k). The transcriptional activity of TRIP13 was detected with luciferase assays. * represented P < 0.05, and *** represented P < 0.001 compared with control or indicated groups, calculated by T-test in (j, h and k). Spearman correlation analysis was performed in (c, e and g). Analyzed data were from three independent experiments, and shown as means± SEM

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