Jinkai Liu

Supplementary Figure 10 shows the effects of B. fragilis conditioned medium (CM) on HCC cells, construction of Enolase-overexpressing E. coli MG1655 strain, and the important role of Vimentin in B. fragilis mediated HCC promotion.

Supplementary Figure 2 shows the association between the liver dysfunction and gut/liver microbial dysbiosis.

Supplementary Figure 1 shows the comparison of the biochemical parameters between the HCC patients and healthy subjects.

Supplementary Figure 11 shows that the gut dysbiosis in HCC patients compromises intestinal barrier integrity, enabling the translocation of live pathobionts such as B. fragilis to the liver. Multisite biopsy analysis of the intrahepatic microbiome and host transcriptome revealed that the presence of gut pathobionts in tumor regions positively correlated with the expression of host cytokines and oncogenes. Concordantly, oral gavage of B. fragilis in multiple HCC mouse models exacerbated cell proliferation and activated pro-inflammatory and oncogenic signaling pathways that drive hepatocarcinogenesis.

Supplementary Figure 5 shows the B. fragilis-surrounded immune characterization by co-detection by indexing (CODEX) multiplexed staining, combined with 16S rRNA FISH for B. fragilis detection.

Supplementary Figure 3 shows the Sstool and hepatic microbiome profiles.

Supplementary Figure 4 shows the intrahepatic microbiome heterogeneity in association with host gene transcription.

Supplementary Figure 6 shows that the fecal microbiota transplantation (FMT) of HCC stool to germ-free mice promotes gut barrier disruption.

Supplementary Figure 7 shows that the fecal microbiota transplantation (FMT) of HCC stool to germ-free mice promotes liver inflammation.

Supplementary Table 1 shows the study participant's characteristics; Supplementary Table 2 shows the taxa with increased/decreased abundance in the HCC stool samples compared with healthy stool samples; Supplementary Table 3 shows the enrichment analysis of taxa presence/absence in the liver tissue; Supplementary Table 4 shows the association between the genes and intrahepatic taxa based on the LASSO regression; Supplementary Table 6 shows the Enrichment analysis of gene component of penalized CCA; Supplementary Table 7 shows the summarized intrahepatic taxa mapping of each HCC patient; Supplementary Table 8 shows the gene-HVT correlations for HCC patients harboring HVT and HCC patients harboring non-HVT; Supplementary Table 9 shows the colony identification by Sanger sequencing; Supplementary Table 10 shows the pathway enrichment analysis for mice PCR array; Supplementary Table 11 shows the protein mass spectrometry identification; Supplementary Table 12 shows the 16S qPCR result for real and negtive controls; Supplementary Table 13 shows the antibodies used in this study.