Fig. 5

IGF2BP1 binds with 3′UTR of ERRα to increase its mRNA stability. The binding between ERRα mRNA and potential reader proteins in MG-63 (a) or HOS (b) cells was checked by RIP-PCR; the binding between ERRα mRNA with YTHDF2 or IGF2BP1 in parental or Dox-resistant MG-63 (c) and HOS (d) cells were checked by RIP-PCR; e the expression of IGF2BP1 in Dox-resistant and parental OS cells were checked by western blot analysis; f The expression of IGF2BP1 and ERRα in sh-Control and sh-IGF2BP1 Dox-resistant OS cells were checked by western blot analysis; the mRNA of ERRα in sh-Control and sh-IGF2BP1 MG-63/Dox (g) or HOS/Dox (h) cells treated with Act-D for different time periods; i cells were transfected with vector control (pcDNA) or pcDNA/IGF2BP1 for 24 h, and then the expression of IGF2BP1 and ERRα were checked by western blot analysis; MG-63 (j) or HOS (k) cells were transfected with vector control (pcDNA) or pcDNA/IGF2BP1 for 24 h, and then further treated with increasing concentrations of Dox for 24 h. Data are presented as means ± SD from three independent experiments. ^**p < 0.01 by Student’s t test