Extended Data Fig. 2: Individual HCC patient fecal microbiota initiates liver precancerous lesions in germ-free mice without DEN treatment.
(a) Design of FMT experiment to germ-free mice without DEN treatment (GF/PBS group n=6; GF/HD-FMT group n=12; GF/HCC-FMT group n=16). (b) Representative images of liver gross morphology (yellow circles indicate nodules), and H&E staining of mice liver sections with incidence of dysplasia and nodules number statistical results. n=6 (GF/PBS), 12 (GF/HD-FMT), 16 (GF/HCC-FMT). (c) IHC staining for PCNA and Ki-67. n=6 biologically independent samples. (d) Hepatic infiltration of Th1, Th17, and Th2 cells was evaluated by flow cytometry. n=3 biologically independent samples. (e) Desmin and α-SMA IHC staining, and Sirius red staining of liver sections. n=6 biologically independent samples. (f) Mouse Cancer Pathway Finder Array and (g) Inflammatory Response and Autoimmunity PCR Array of liver tissues. f and g, n=3 independent experiments with similar results. Data (excluding incidence of dysplasia and PCR array results) are presented as mean ± SEM. Each data point in bar plots represents one mouse. Incidence of dysplasia was calculated using Fisher’s exact test. Unless otherwise stated, statistical significance was calculated using one-way ANOVA. Adjustments were made for multiple comparisons.
