Fig. 4: Common fecal 16S rRNA-related signatures in three independent models of prostate cancer. | Nature Communications

Fig. 4: Common fecal 16S rRNA-related signatures in three independent models of prostate cancer.

From: The gut microbiome-prostate cancer crosstalk is modulated by dietary polyunsaturated long-chain fatty acids

Fig. 4

a Differential enrichment of bacterial genera from mice with TRAMP-C2 tumours at the end point growth stage (late tumour growth) and the baseline before tumour cell injection (n = 8 mice/group). b Differential enrichment of bacterial genera corresponding to mice with Pten−/−; Rb1−/− tumours and tumour-free mice (n = 8 mice/group). c Relative abundance, in percentage (%) of total 16S rRNA sequences, of Parabacteriodetes 16S rRNA (left, p = 0.003 (Active growth) and p = 0.02 (End point), Welch’s t-test) and Lactobacillus 16S rRNA (right, p = 0.05 (Active growth), Welch’s t-test) from fecal samples of mice with TRAMP-C2 tumour harvested at different stages of prostate cancer development (n = 8 mice/group). d Relative abundance, in % of total 16S rRNA sequences, of Parabacteriodetes 16S rRNA (left, p = 0.02, Welch’s t-test) and Lactobacillus 16S rRNA (right, p = 0.003 (Pten−/−; Rb1+/+) and p = 0.04 (Pten−/−; Rb1−/−), Welch’s t-test) from fecal samples of mice without tumour, with Pten−/−; Rb1+/+ or Pten−/−; Rb1−/−, tumours (n = 8 mice/group). e Ven diagram of a PICRUSt analysis of functions predicted to be enriched in fecal samples from TRAMP-C2 tumours at end point compared to baseline controls. The enrichment of predicted function was also performed for Pten−/−; Rb1+/+ and Pten−/−; Rb1−/− tumours and compared to no-tumour controls is also shown. f The 7 predicted functions between fecal tumour samples and controls that were commonly enriched between mice bearing TRAMP-C2, Pten−/−; Rb1+/+ and Pten−/−; Rb1−/− tumours, following a PICRUSt analysis are displayed. Graphs in (a, b) are mean ± SD. Graphs in (c, d) are mean ± SEM, Welch’s t-test.

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