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. Author manuscript; available in PMC: 2020 Aug 1.
Published in final edited form as: Mol Cancer Res. 2019 May 20;17(8):1652–1664. doi: 10.1158/1541-7786.MCR-19-0144

Figure 3 – Isogenic cells show wild-type TP53 presence rescues proliferation defects from TPRKB knockdown.

Figure 3 –

A) TPRKB was stably knocked down in isogenic HCT116 (TP53 wild-type) and HCT116 TP53WT/R248W cells. The stable clones were assayed for cell proliferation and tumor formation in nude mice. B) TPRKB knockdown by shRNA was performed in H358 cells stably expressing LacZ control (left) or TP53 (right) and proliferation was monitored. Inset Western blot panels confirm TP53 over-expression from lentiviral transduction and TPRKB knockdown. All experiments utilized triplicate samples, with the average and standard error plotted.

* indicate p-values < 0.05 and ** indicate p-values <0.01.