Fig. 6: HMGA1 promotes DNA repair through the regulation of RAD51expression in CCA cells.
From: Overexpression of HMGA1 confers radioresistance by transactivating RAD51 in cholangiocarcinoma
A, B Immunofluorescence staining of γ-H2AX was measured in HUCTT1 cells transfected with sh-HMGA1, RAD51 and control vectors at different times (0 h, 2 h, 6 h, 12 h, and 24 h) after 2 Gy X-ray radiation. C Immunofluorescence staining of γ-H2AX was measured in HUCTT1 cells transfected with HMGA1 overexpression or control plasmid with or without RAD51 inhibitor (B02 9 μM) at different times (0 h, 2 h, 6 h, 12 h, and 24 h) after 2 Gy X-ray radiation. D Western blot analysis of γ-H2AX protein levels in HUCCT1 cells transfected with sh-HMGA1, RAD51 and control vectors at different times (0 h, 2 h, 4 h, and 6 h) after 8 Gy X-ray radiation. E Western blot analysis of γ-H2AX protein levels in HUCCT1 cells transfected with HMGA1 overexpression plasmid or control plasmid with or without RAD51 inhibitor (B02 9 μM) at different times (0 h, 2 h, 4 h, and 6 h) after 8 Gy X-ray radiation. F, G A comet assay was performed in HUCCT1 cells transfected with sh-HMGA1, RAD51 and control vectors at 12 h after 2 Gy X-ray radiation. H A comet assay was performed in HUCCT1 cells transfected with HMGA1 overexpression plasmid or control plasmid with or without RAD51 inhibitor (B02 9 μM) at 12 h after 2 Gy X-ray radiation. I, J The frequencies of MN in HUCCT1 cells transfected with sh-HMGA1, RAD51 and control vectors at 24 h after 4 Gy X-ray. K, L The frequencies of MN in HUCCT1 cells transfected with HMGA1 overexpression plasmid or control plasmid with or without RAD51 inhibitor (B02 9 μM) at 24 h after 4 Gy X-ray. Yellow arrows indicate MN-γH2AX+; white arrows indicate MN-γH2AX−. The significant differences between the two groups were analyzed by Student’s t test. *P < 0.05, **P < 0.01.
