Role of signaling pathways in the interaction between microbial, inflammation and cancer

Abstract Microbial-induced inflammation serves a dual role, safeguarding against pathogens but also posing a risk of secondary harm to host tissues, potentially leading to fibrosis and cancer. Beyond traditional pathogens, gut microbiota, the mutualistic microorganisms inhabiting the gastrointestinal tract, crucial for digestion, immunity, and cancer prevention, can incite inflammation-related cancer when their microenvironment undergoes changes. Recent research reveals that microbiota members like Escherichia coli and other genotoxic pathogens can induce DNA damage across various cell types. Chronic infections involving microbiota members like Helicobacter spp., linked to liver, colorectal, cervical cancers, and lymphoma, can activate carcinogenic processes. Inflammatory responses, driven by immune cells releasing inflammatory molecules like macrophage migration inhibitory factor (MMIF), superoxide peroxynitrite, pro-inflammatory cytokines, adhesion molecules, and growth factors, contribute to DNA damage and oncogenic mutations accumulation. This microenvironment further supports neoplastic cell survival and proliferation. This summary discusses the involvement of inflammatory pathways in microbial-triggered carcinogenesis and the potential role of microbiota modulation in cancer prevention.