Fig. 6

circPTK2 promotes HCC cells proliferation, migration, and invasion via AKR1C3. (A) The protein level of AKR1C3 in HCC-LM3 and MHCC 97-H cells transfected with sh-circPTK2 plasmid alone or co-transfected with AKR1C3 overexpression vectors. (B,C) Cell viability of HCC-LM3(B) and MHCC 97-H (C) transfected with sh-circPTK2 plasmid alone or co-transfected with OE-AKR1C3 plasmids, measured by CCK8 (Mean ± SD, n = 6, ***p < 0.001). (D,E) Clone forming capacity of HCC-LM3 (D) and MHCC 97-H (E) cells co-transfected with sh-circPTK2 and OE-AKR1C3, evaluated by colony formation assays (Mean ± SD, n = 3, ***p < 0.001). (F,G) EdU assays estimated the DNA replication capacity of HCC-LM3(F) and MHCC 97-H (G) cells transfected with sh-circPTK2 plasmid alone or co-transfected with OE-AKR1C3. Mean ± SD, n = 3, ***p < 0.001, scale bar: 100 μm. (H–J) The cells migration of HCC-LM3 and MHCC 97-H co-transfected with sh-circPTK2 and OE-AKR1C3, assessed by scratch-healing experiments (H,I) and transwell migration assays (J). Mean ± SD, n = 3, **p < 0.01, ***p < 0.001, scale bar:100 μm. (K) The invasion ability of HCC-LM3 and MHCC 97-H co-transfected with sh-circPTK2 plasmid and OE-AKR1C3 vector, measured by transwell invasion assays. Mean ± SD, n = 3, **p < 0.01, ***p < 0.001.