Research Paper Volume 12, Issue 23 pp 24424—24440

FOXM1/DVL2/Snail axis drives metastasis and chemoresistance of colorectal cancer

class="figure-viewer-img"

Figure 1. The role of FOXM1 in metastasis and drug-resistance of CRC cells. (A) The sensitivities of HCT-8 and HCT-8/L-OHP cells to oxaliplatin were assessed using MTT assays. (B) The IC50 of oxaliplatin in HCT-8 and HCT-8/L-OHP cells. (C) The sensitivities of HCT-8 and HCT-8/VCR cells to vincristine. (D) The IC50 of vincristine in HCT-8 and HCT-8/VCR cells. (E) The migratory and invasive behaviors of HCT-8, HCT-8/L-OHP and HCT-8/VCR cells were examined using transwell and matrigel invasion assays. (F) Western blotting for FOXM1 expression in HCT-8, HCT-8/L-OHP and HCT-8/VCR cells. GAPDH was used as the internal control, and the relative quantitation of FOXM1 expression was normalized against GAPDH using Image J analysis. The oxaliplatin sensitivity and IC50 (G, H), as well as the vincristine sensitivity and IC50 (I, J) in HCT-8 cells transfected with pcDNA3.1 or pcDNA3.1-FOXM1. (K, L) The oxaliplatin sensitivity and IC50 in HCT-8/L-OHP cells transfected with shNC or shFOXM1. (M, N) The vincristine sensitivity and IC50 in HCT-8/VCR cells transfected with shNC or shFOXM1. The migratory and invasive behaviors were examined using transwell and matrigel invasion assays in HCT-8 cells transfected with pcDNA3.1 or pcDNA3.1-FOXM1 (O), in HCT-8/L-OHP and HCT-8/VCR cells transfected with shNC or sh-FOXM1 (P, Q). Data are expressed as mean ± SD of three independent experiments. *P < 0.05.