Extended Data Fig. 2: Effect of PCSK9 re-expression and the host immune system on tumour formation by PCSK9-knockout cells.
From: Inhibition of PCSK9 potentiates immune checkpoint therapy for cancer
a, Western blot analysis of the expression of exogenously transduced, HA-tagged PCSK9 in PCSK9KO B16F10 cells. The analysis was done once. b, c. Tumour formation from B16F10 PCSK9KO cells transduced with either vector control or PCSK9 (b), and Kaplan–Meier survival curves of host mice (c). About 2 × 105 tumour cells were injected subcutaneously into C57BL/6 mice and observed for tumour formation. n = 5 tumours per group. Error bars show means ± s.e.m.; P-values were determined by two-way ANOVA in b and log-rank test in c. d–i, Growth rate (d, g), host survival (e, h) and endpoint tumour weight (f, i) of vector control and PCSK9KO 4T1 (d–f) and B16F10 (g–i) tumours. In each case, about 1 × 105 tumour cells were injected subcutaneously and observed for tumour formation in NCG mice. n = 6 mice for d, e, g, h; and n = 5 tumours for f, i. Error bars in d, f, g, i represent means ± s.e.m.; ns, not significant, as determined by two-way ANOVA (d, g), log-rank test (e, h), or unpaired two- sided t-test (f, i). j, k, Tumour growth from vector control and PCSK9KO B16F10 cells in Rag1−/− C57BL/6 mice (j) and Kaplan–Meier survival curve of tumour-bearing host mice (k). About 1 × 105 vector control or PCSK9KO B16F10 tumour cells were injected into Rag1−/− C57BL/6 mice and observed for tumour formation. n = 5 tumours per group. Error bars in j show means ± s.e.m. P-values were calculated by two-way ANOVA in j and by log-rank test in k.
