Figure S1.
Panel A shows a schematic of the CRISPR/Cas9 expression plasmid, highlighting the sequence corresponding to the selected TNFR1 gRNA. Panel B includes flow cytometry histograms and line graphs showing tumor size over time for Panc02 wild-type (WT) and TNFR1 knockout (KO) variants. The histograms compare isotype control, WT, and KO clones, while the line graphs depict tumor growth trends. Panel C presents similar data for LLC WT and TNFR1KO variants, with histograms and line graphs showing tumor size over time. Panel D shows data for 4T1 WT and TNFR1KO variants, including histograms and line graphs of tumor growth. Panel E includes histograms and line graphs for B16F10 WT and TNFR1KO variants, illustrating tumor size over time. Panel F features line graphs assessing the proliferation of EO771 and MC38 WT and TNFR1KO variants using Incucyte, with relative cell confluence plotted over time.
Knocking down TNFR1 in transplantable murine tumor cell lines. (A) CRISPR/Cas9 expression plasmid used to silence TNFR1 expression. The sequence in the dotted square corresponds to the selected TNFR1 gRNA. (B–E) Similar experiments as in Fig. 1, A–D with TNFR1 WT and KO variants derived from the Panc02, LLC, 4T1, and B16F10 tumor cell lines (two-way ANOVA statistical comparisons) (n = 6). (F) Incucyte assessment of proliferation of the indicated WT or TNFR1KO variants of EO771 (left) and MC38 (right). P < 0.01 (**) and P < 0.0001 (****).