Figure 1.

Interactions between microbiota and esophageal carcinogenesis. This figure visually summarizes the complex interactions between various microbiota and their impact on EC pathogenesis, focusing on ESCC. It highlights esophageal microbiota dysbiosis, with pathogenic bacteria activating carcinogenic pathways. The diagram also depicts beneficial SCFAs-producing bacteria and harmful LPS-producing bacteria within the gut microbiota. Oral microbiota, including Tannerella forsythia, Streptococcus anginosus, Aggregatibacter actinomycetemcomitans, Fusobacterium mucleatum and Porphyromonas gingivalis, influence EC development. Central to the figure is the signaling cascade initiated by bacterial LPS interacting with TLRs on esophageal cancer cells. LPS from Gram-negative bacteria activates TLR4, while other microbial components stimulate TLR1/2/6 and TLR9, signaling through the adaptor protein MyD88. This activation leads to downstream inflammatory responses via the NF-κB pathway, inducing cytokines (IL-1β, IL-6, IL-8, TNF-α) that promote tumor cell proliferation, angiogenesis, invasion, and the expression of COX-2 and NLRP3, which are involved in inflammation and pyroptosis. The figure also illustrates how Fusobacterium nucleatum and Porphyromonas gingivalis specifically contribute to EC progression. Porphyromonas gingivalis interacts with the IL-6 receptor, activating JAK2/STAT3 signaling, which drives cell proliferation and migration. Fusobacterium nucleatum promotes inflammation and tumor invasion via NF-κB and NOD-like receptor signaling pathways. The interplay between these microbial factors and the host immune response underscores the potential of the microbiota as targets for cancer therapy and diagnostics. (Drawn by FigDraw).