Fig. 2: Distinct biological roles of TET1 in thyroid cancer in vitro and in vivo.
From: Hypoxia switches TET1 from being tumor-suppressive to oncogenic
A Western blot analysis of TET1 and dot blot of genome 5-hmC in 8505C and K1 cells treated with/without Dox. Methylene blue staining of the membrane showing the DNA loading. Cell proliferation (B), colony formation (C) and cell migration (D) assays were performed to examine the effect of ectopic expression of TET1 in 8505C and K1 cells by doxycycline (Dox)-inducible gene expression system (Tet-On). E Western blot and dot blot assays were performed for TET1-knockout C643 cells and control cells. A real-time cell analyzer (RTCA) was used to monitor the proliferation (F) and migration (G) of the above cells. H Western blot and dot blot assays showing Tet1 expression and 5-hmC levels in mice with different genotypes. I Survival rates (table in the upper panel) and survival curves (lower panel) of mice with different genotypes during the 100-day breeding. J Body weight of the indicated mice. Plots and error bars indicate the mean and SD values recorded weekly. K Representative pictures and weight of thyroid tumors at the 100th day. L Comparison of iodine uptake rate of thyroid in mice with different genotypes. Dox− negative control, Dox+ cells inducibly expressing TET1. sgCon control cells, sgTET1 TET1-knockout C643 cells. Brafm/+ Braf heterozygous mutation, Tet1+/+ Tet1 wild-type, Tet1−/− Tet1 homozygous deletion. Graph shows mean ± SD. Statistical analysis was performed by unpaired Student’s test. **p < 0.01.
