A Narrative Review on Unravelling Bacterial‐Mediated Carcinogenesis and Possible Alternative Treatment Strategies
Abstract
The potential roles of chemical, physical, and viral factors in cancer development are well documented. Similarly, bacterial carcinogenesis has been reported previously, though not extensively. Therefore, we aimed to provide comprehensive, mechanistic evidence on the pathogenesis of bacteria-induced carcinogenesis and possible treatments to halt cancer progression. Infections by bacteria, including Salmonella typhi, Fusobacterium spp., Chlamydia pneumoniae, Staphylococcus aureus, Helicobacter pylori, and Mycobacterium tuberculosis, have been reported as the most common carcinogenic bacteria in humans. These bacteria can produce toxins and carcinogenic metabolites those promote the development of cancer in a variety of ways, including by changing the dynamics of the cell cycle, triggering signaling pathways in the cell, such as NF-κB, MAPK, PI3K-PKB/Akt, and JAK/STAT, and activating anti-apoptosis activities by increasing Bcl-2 and decreasing BAX, and caspases expression along with suppressing p53 and pRb tumor suppressor proteins. Moreover, inflammatory cytokines such as tumor necrosis factor-α (TNF-α), interferon-gamma (INF-γ), interleukin-1β (IL-1β), IL-4, IL-6, IL-10, IL-1, IL-17, IL-23, and other inflammatory cytokines are a few of the factors that promote chronic inflammation and initiate carcinogenesis. In addition, bacterial infection can generate free radicals that induce DNA damage, thereby promoting carcinogenesis. Following these mechanisms, bacteria can cause a…
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