Fig. 7

SKA3 promoted CCA cell proliferation and fatty acid synthesis via the PARP1/HIF-1a axis under hypoxic conditions. A Knockdown of PARP1 or HIF-1a reversed the proliferation rate of SKA3 overexpression CCA cells under hypoxic conditions. B Clone-formation ability of CCA cells was promoted by SKA3 overexpression and rescued by knockdown of PARP1 or HIF-1a under hypoxic conditions. C Flow cytometry analysed cell cycle of CCA cells transfected with NC, LV-SKA3, SKA3 overexpression cells transfected with Si-PARP1 and SKA3 overexpression cells transfected with Si-HIF-1a. D Cellular neutral lipids were measured in QBC939 cells by double staining with Nile Red and DAPI. E Cellular triglycerides were measured in QBC939 cells, normalizing by NC group. F Western blotting analysis of fatty acid synthesis markers. G The ATP concentration in QBC939 cells were tested by ATP Assay Kit. H Xenograft tumours in nude mice generated with QBC939 cells. I-J Growth of xenografts was promoted in SKA3 overexpression group and rescued in SKA3 overexpression transfected with Si-PARP1 or Si-HIF-1a group. K Intensity of Nile red staining and the expression of SKA3, PARP1, HIF-1a and Ki-67 in different groups of xenografts (scale bar: 50μm). *P < 0.05, **P < 0.01, ***P < 0.001