Abstract
Human gut microbiota contains a large, complex, dynamic microbial community of approximately 1014 microbes from more than 1,000 microbial species, i.e., equivalent to 4 × 106 genes. Numerous evidence links gut microbiota with human health and diseases. Importantly, gut microbiota is involved in the development and function of the brain through a bidirectional pathway termed as the gut-brain axis. Interaction between gut microbiota and immune responses can modulate the development of neuroinflammation and cancer diseases in the brain. With respect of brain cancer, gut microbiota could modify the levels of antioxidants, amyloid protein and lipopolysaccharides, arginase 1, arginine, cytochrome C, granulocyte–macrophage colony-stimulating factor signaling (GM-CSF), IL-4, IL-6, IL-13, IL-17A, interferon gamma (IFN-γ), reactive oxygen species (ROS), reactive nitrogen species (e.g., nitric oxide and peroxynitrite), short-chain fatty acids (SCFAs), tryptophan, and tumor necrosis factor-β (TGF-β). Through these modifications, gut microbiota can modulate apoptosis, the aryl hydrocarbon receptor (AhR), autophagy, caspases activation, DNA integrity, microglia dysbiosis, mitochondria permeability, T-cell proliferation and functions, the signal transducer and activator of transcription (STAT) pathways, and tumor cell proliferation and metastasis. The outcome of such interventions could be either oncolytic or oncogenic. This review scrutinizes the oncogenic and oncolytic effects of gut microbiota by classifying the modification mechanisms into (i) amino acid deprivation (arginine and tryptophan); (ii) kynurenine pathway; (iii) microglia dysbiosis; and (iv) myeloid-derived suppressor cells (MDSCs). By delineating the complexity of the gut-microbiota-brain-cancer axis, this review aims to help the research on the development of novel therapeutic strategies that may aid the efficient eradication of brain cancers.
Highlights
The incidence of primary brain cancer is estimated to be 7.2–12.5 per 100 million persons per year, accounting for up to 2% and 23% of all adults and childhood cancers, respectively (Wrensch et al, 2002; Marie and Shinjo, 2011)
Understanding the mechanisms of involvement of the gut microbiota-brain axis in the development or suppression of brain tumor could establish a new insight for the generation of novel anti-tumor therapeutic interventions
By providing state-of-the-art information on the gut-microbiota-brain-cancer axis, this review aims to help cancer researchers and clinicians with the development of novel anti-tumor therapeutic strategies
Summary
The incidence of primary brain cancer is estimated to be 7.2–12.5 per 100 million persons per year, accounting for up to 2% and 23% of all adults and childhood cancers, respectively (Wrensch et al, 2002; Marie and Shinjo, 2011). It has been suggested that some internal factors (i.e., genetic elements such as POT1) and external factors (i.e., environmental factors such as ionizing irradiation) could increase the risk of brain tumors (Picano et al, 2012; Robles-Espinoza et al, 2014). It is well-known that some microorganisms have oncogenic or oncolytic activity on tumor cells. Understanding the mechanisms of involvement of the gut microbiota-brain axis in the development or suppression of brain tumor could establish a new insight for the generation of novel anti-tumor therapeutic interventions. The gut-brain axis represents a complex multidirectional network between the gastrointestinal (GI) tract microbiota, the enteric nervous system, and the brain that influences immune responses, inflammation processes, and metabolic functions (Fung et al, 2017; Dehhaghi et al, 2019a)
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