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. 2021 Mar 15;14(6):101059. doi: 10.1016/j.tranon.2021.101059

Fig. 4.

Fig 4

IRF2 overexpression decreases lenvatinib sensitivity and cellular apoptosis of HCC cells. A. Immunoblotting of cleaved Caspase-3, survivin, C-myc, Cyclin-D1, IRF2 and β-catenin in control and IRF2-knockdown HepG2 cells treated with 7.5 µM of lenvatinib for 48 h. β-actin was used as loading control; B. mRNA levels of IRF2 and β-catenin in control and IRF2-knockdown HepG2 cells treated with 7.5 µM of lenvatinib for 48 h as described in Fig. 4a. β-actin was used as loading control. Student's t-test; C. Immunofluorescence staining of TUNEL (green) and DAPI (blue) in control and IRF2-knockdown HepG2 cells treated with 7.5 µM of lenvatinib for 48 h; D. Cell viability of control and IRF2-knockdown HepG2 cells treated with 0, 2.5, 5, 7.5, 10, 15 µM of lenvatinib for 48 h. Student's t-test; E. Immunoblotting of cleaved Caspase-3, survivin, C-myc, Cyclin-D1, IRF2 and β-catenin in control and IRF2-overexpressing Huh7 cells treated with 7.5 µM of lenvatinib for 48 h. β-actin was used as loading control; F. mRNA levels of IRF2 and β-catenin in control and IRF2-overexpressing Huh7 cells treated with 7.5 µM of lenvatinib for 48 h as described in Fig. 4e. β-actin was used as loading control. Student's t-test; G. Cell viability of control and IRF2-overexpressing Huh7 cells treated with 0, 2.5, 5, 7.5,10, 15 µM of lenvatinib for 48 h. Student's t-test.