Extended Data Fig. 7: A low-BCAA diet restrains PCa progression as a dietary intervention approach.
a-c. The BCAA concentration (a), body weight (b) and daily food intake (c) in normal or high-BCAA diet treated PtenPC−/− mice (n = 7 mice per group). Data represent the mean ± SEM. Statistical significance was determined by two-tailed unpaired t-test (a and c) and two-way ANOVA followed by multiple comparisons test (b), NS, no significance. d. H&E and IHC staining for Ki67, αSMA and CK8 in prostate sections from the indicated mice and quantification of Ki67 and αSMA positivity (n = 10 tumors each group). Data represent the mean ± SEM. Statistical significance was determined by two-tailed unpaired t-test (up) and two-sided Fisher’s exact test (bottom). Scale bar, 100 μm. e. H&E and AR staining of lymph nodes from 5-month-old PtenPC−/− mice fed an NCD or a high-BCAA diet (n = 15 mice per group; the P value was determined by two-sided Fisher’s exact test). Scale bar, 100 μm. Scale bar, 100 μm. (f-h) The plasma BCAA concentration (f), body weight (g) and daily food intake (h) in normal and a low-BCAA diet treated PtenPC−/−; Tp53PC−/− mice (n = 7 mice per group). Data represent the mean ± SEM. Statistical significance was determined by two-tailed unpaired t-test (f and h) and two-way ANOVA followed by multiple comparisons test (g), NS, no significance. i. Measurement of BCAA and oxidative phosphorylation metabolites in PDXs transplanted into 6-week-old NSG mice fed an NCD or a low-BCAA diet for 7 weeks (n = 3 biological replicates per group).
