Research Paper Volume 12, Issue 13 pp 13059—13075
Loss of AKR1B10 promotes colorectal cancer cells proliferation and migration via regulating FGF1-dependent pathway
Figure 5. AKR1B10 inhibits CRC cell growth in an FGF1-dependent manner. (A) Immunoblot showing AKR1B10, FGF1 and GAPDH protein levels in HT29 cells transfected with AKR1B10-shRNA and in HCT116 cells transfected with AKR1B10 overexpression plasmid. (B) Immunoblot showing AKR1B10, FGF1 and GAPDH protein levels in HT29 transfected with FGF1-shRNA alone or in combination with AKR1B10-shRNA. (C–E) Proliferation rates (C), colony forming capacity (D) and migration rates (E) of the HT29 cells transfected as above. Data are presented as mean ± SD. NC, negative control; KD, AKR1B10-shRNA; VEC, vector; OE, AKR1B10 overexpression plasmid. “-”, control-shRNA. “+”, AKR1B10 or FGF1 shRNA. *P < 0.05, **P < 0.01, ***P < 0.001.