Extended Data Fig. 2: LDHA-deficient tumour model for neoadjuvant CTLA-4 blockade treatment.
From: CTLA-4 blockade drives loss of Treg stability in glycolysis-low tumours
a, Expression of LDHA in 4T1-KD and 4T1-Sc whole-cell protein extracts by western blot analysis. Vinculin was used as a loading control. Representative of three independent experiments. b, Glycolytic proton efflux rate (glycoPER) in 4T1-KD and 4T1-Sc cultures (n = 20). 2-DG, 2-deoxy-d-glucose; Rot/AA, rotenone plus antimycin A. c, In vivo growth of 4T1-KD and 4T1-Sc tumours orthotopically implanted in the mammary fat pad of immunocompetent wild-type (WT) and immunodeficient RAG2-knockout (KO) BALB/c mice (n = 10 mice per group; representative of two independent experiments). d, Growth of primary 4T1-Sc and 4T1-KD tumours in mice treated as in Fig. 2a (left) and average tumour diameter on the day of tumour resection (right) (IgG, n = 9; anti-CTLA-4, n = 12). e, LDH activity in 4T1-Sc (n = 4) and 4T1-KD (n = 5) tumour extracts on the day of tumour resection after treatment as in d. f, Tumour growth after a second injection with 4T1-Sc in 4T1-KD- and 4T1-Sc-bearing mice that survived neoadjuvant treatment with CTLA-4 blockade as in Fig. 2a (n = 4 per group, except for naive, n = 5). Data are mean ± s.d. (b) or mean ± s.e.m. (c–f). P values determined by two-way ANOVA with Bonferroni correction (b, c, f) or two-sided unpaired t-test (e).
