Fig. 2
CGN c.3560C > T leads to oxaliplatin resistance in cancer cells. A, Dyk-CGN c.3560 C > C or c.3560C > T were transient transfection in HT-29 cells and treated with different concentrations of oxaliplatin (0 μM, 1 μM, 2 μM, 4 μM, 8 μM, and 16 μM) for 24 h for the MTT assay. The IC50 values of oxaliplatin in HT-29 cells were measured by MTT assay. Value, mean ± SEM from analysis of three different clones. B, Representative images showing tumor growth in Luc-CGN c.3560 C > C and c.3560C > T HT-29 orthotopic xenograft tumor receiving saline and oxaliplatin treatment were assessed by IVIS system. Mice were repeatedly imaged until week four after inoculation to record luminescence signals. The data were shown as radiance (photons/ sec/ cm2/ steradian) with a color bar. C, Quantitative analysis of luminescence intensity from each tumor. Mice were analyzed by optical bioluminescence imaging at 1, 7, 14, 21, and 28 days after cancer cell injection. Arrows indicate the treatment time points. Value, mean ± SEM, n = 6 in each group. D, Luciferase bioluminescence signal detection of various organs. E, (Upper) The frequencies of pulmonary metastasis were assessed in mice carrying Luc-CGN 3560 C > C or c.3560C > T HT-29 xenograft tumors at the 28th days after injection. Metastasis frequencies based on the number of mice were shown. (Lower) H&E staining results of lung tissues in CGN c.3560 C > C group and CGN c.3560 C > T group. Melanoma foci formed in the lungs were observed in CGN c.3560 C > T group (black arrows). Original magnification, × 10, scale bar, 100 μm. Data are presented as the mean ± SEM. t-test for statistical significance, *p < 0.05.; N.S, ≥ 0.05, not significant