Pediatric hepatoblastoma model hints at DNA damage repair pathway for novel therapeutics NatureComms
with regression of replicate and number of genes per spot. Dimensionality reduction and clustering were performed with principal component analysis using the default setting in function RunPCA. We integrated the spatial data with scRNA-seq data by using the cell clusters inferred by LCA from scRNA-seq dataset as a reference. Spatial feature expression plots were generated using Seurat’s SpatialFeaturePlot.Cells were seeded at a density of 100, 000 cells in each well in 6 well plates.
cell was cultured with DMEM complete medium for 5 days and HepG2 was cultured with DMEM complete medium for 8 days. The culture medium and AZD7648 and doxorubicin were changed every 2–3 days. After removing media, cells were washed with Dulbecco’s phosphate buffered saline without calcium or magnesium and fixed with 4% formaldehyde in PBS for 20 min. Once formaldehyde was removed, cells were stained with 0.1% crystal violet for 1 h. Plates were rinsed with water and imaged.
and HepG2 cells were seeded in 96-well plates. After 24 h, cells were treated with AZD7648 and doxorubicin in an 8 × 5 matrix. Cells were treated for 5 days, and cell viability was determined using the PrestoBlue assay according to manufacturer’s instructions. Cell viability for each treatment was normalized against the control group. A Bliss independence model was used to evaluate combination effects.
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