靶向抑制CDK12/13在高级别胶质瘤中的体外治疗效果和作用分子机制探究
In vitro therapeutic effects and molecular mechanisms of targeted inhibition of CDK12/13 in high-grade gliomas
Note： A. Western blotting analysis of CDK12 expression levels in aGBM (U251), pGBM (SF188, KNS42), and DIPG17 cell lines after CDK12 knockout by using CRISPR-Cas9 system. B. Detection of cell viability of U251, SF188 and KNS42 on the fourth day, and DIPG17 on the seventh day after CDK12 knockout by CellTiter-Glo. C. Dot plot (upper) and bar chart (below) of neurosphere assay of DIPG17 cells. Fifty or 100 DIPG17 cells were seeded in each well (96-well plate) following CDK12 knockout. After 14 d of culture, the number of neurosphere was counted and mapped. D. Scanogram (left) and cartogram (right) of colony formation assay of CDK12-knockout GBM cell lines (U251, SF188 and KNS42). Cells were plated at 2 000 per well (six well plate), with half-volume mediumeing changed every 4 d, followed by crystal violet staining, photographing and counting in two weeks. ①P=0.000 2, ②P=0.000 4, ③P=0.000 1, ④P=0.008 7, ⑤P=0.001 4, ⑥P=0.004 0, ⑦P=0.002 9,⑧P<0.000 1.
