Additional file 2: of Nuciferine inhibits the progression of glioblastoma by suppressing the SOX2-AKT/STAT3-Slug signaling pathway

Figure S1. Effect of NF on the viability of U87MG and U251 cells. Fig S2. Cell viability of normal human cells after treatment with different concentrations of NF (0–180 μM, 48 h). Fig S3. Apoptosis of GBM cells after treatment with NF (0–150 μM, 24 h). Fig S4. NF suppressed HIF1A and VEGFA in GBM cells. Fig S5. Multiple gene comparisons in GBM: CD133, CD44, Oct4, SOX2, Nanog, ALDH1A1, Olig2, and Nestin (GEPIA). Fig S6. Subcellular localization of SOX2. Fig S7. Subcellular localization of Nestin and CD44 (HPA, human protein atlas). Fig S8. OS and DFS of GBM patients based on SOX2 expression. Fig S9. The expression of SOX2 in GBM cells treated with NF. Fig S10. Immunofluorescence assay (Scale bar: 200 μm) of SOX2 after treatment with NF (30 μM, 48 h) in U251 cells. Fig S11. Rescue-dependent manner. Fig S13. The prot experiment of SOX2 in U87MG cells. Fig S12. NF (0, 10, and 15 mg/kg, once a day for a total of 2 weeks) inhibited the growth of U251 xenograft tumors in a dose ein expression in excised xenograft tumors was notably reduced by NF (0, 10, and 15 mg/kg, once a day for a total of 2 weeks) in a dose-dependent manner. Fig S14. Pathology changes of angiogenesis. Fig S15. No obvious necrosis was found in xenograft mice internal organs. (DOCX 5899 kb