Surufatinib achieves radiosensitivity in cholangiocarcinoma by suppressing GINS4 expression to induce Ca2+/cAMP signaling activation

Figure 4 Overexpression of GINS4 promotes tumor proliferation and inhibits apoptosis, while surufatinib suppresses GINS4 expression and is associated with radiosensitization. A: The pLenti-GINS4 (OE-GINS4) construct was generated using standard molecular biology techniques. Western blot analysis was performed to detect GINS4 expression levels among different treatment groups in NOZ and TFK-1 cells; control = empty vector control; B: Under conditions of GINS4 overexpression, cell viability was assessed across various treatment groups; C and D: Flow cytometry was employed to evaluate apoptosis in NOZ and TFK-1 cells in OE-GINS4 compared to control cells, with or without SF + 6 Gy treatment. Quantitative analysis of apoptosis rates among different treatment groups is presented in D; E: Clonogenic assays were conducted to assess the proliferative capacity of OE-GINS4 and control cells, with or without SF + 6 Gy treatment. Representative images of colony formation and quantitative analysis of colony counts for different treatment groups in NOZ and TFK-1 cells are shown in E, respectively. All data are presented as mean ± SEM from three independent experiments. ^bP < 0.01, ^cP < 0.001. SF: Surufatinib.