Fig. 7: HMGA1 promotes proliferation and invasion by increasing RAD51 level in CCA cells.
From: Overexpression of HMGA1 confers radioresistance by transactivating RAD51 in cholangiocarcinoma

A, B The effect of RAD51 on the proliferation of CCA cells was examined by EdU and clonogenic assays of HUCCT1 cells. HUCCT1 cells were transfected with HMGA1 overexpression plasmid or control plasmid with or without RAD51 inhibitor (B02 9 μM) (n = 3 biologically independent samples). C Matrigel invasion data showing that inhibition of RAD51 decreased the invasion potential of CCA cells (n = 3 biologically independent samples). D, E EdU and clonogenic assays of HUCCT1 cells transfected with sh-HMGA1 or sh-Control with or without RAD51 overexpression (n = 3 biologically independent samples) showed RAD51 affect the proliferation of CCA cells. F Matrigel invasion data showing the potential of RAD51 to rescue the loss of HMGA1 in CCA cells as indicated (n = 3 biologically independent samples). G The protein levels of RAD51 were measured by western blot in HUCCT1 cells. H Statistical analysis of HMGA1 expression from IHC staining of our tissue microarray. High and low expression indicate the final score of each sample determined by two pathologists based on the intensity and extent of staining across the tissue microarray section. CCA patients were dichotomized into low (Score ≦7) and high (Score >7) RAD51 protein expression groups based on the IHC staining score. The high and low expression groups were separated based on the best cutoff. The P-value was obtained by Student’s t test. The results represent the mean ± S.D. of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001.