Commensal microbes and p53 in cancer progression
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REVIEW
Open Access
Commensal microbes and p53 in cancer progression Ivana Celardo1, Gerry Melino2 and Ivano Amelio2,3*
Abstract Aetiogenesis of cancer has not been fully determined. Recent advances have clearly defined a role for microenvironmental factors in cancer progression and initiation; in this context, microbiome has recently emerged with a number of reported correlative and causative links implicating alterations of commensal microbes in tumorigenesis. Bacteria appear to have the potential to directly alter physiological pathways of host cells and in specific circumstances, such as the mutation of the tumour suppressive factor p53, they can also directly switch the function of a gene from oncosuppressive to oncogenic. In this minireview, we report a number of examples on how commensal microbes alter the host cell biology, affecting the oncogenic process. We then discuss more in detail how interaction with the gut microbiome can affect the function of p53 mutant in the intestinal tumorigenesis. Keywords: Microbiota, p53, Tumour suppression, Oncogenes, Microenvironment
Background In addition to the genetic factors [1], microenvironmental components certainly influence cancer progression and initiation, as clear evidence emerged on the contribution of integration of extrinsic and intrinsic factors in the disease pathogenesis [2, 3]. Genomic studies have clarified the genetic basis for several malignancies [4–6], as for examples neuroblastoma, which shows a clear pattern of mutations with a well-defined prognostic value [7–11]. In a wider perspective, however, distal interaction among different organs can also contribute to pathogenesis of cancer. The gut microbiota has emerged as determinants not only for the health of gastrointestinal tract (GI), but also for distal districts such as brain, pancreas and liver [12–15]. Causative links between dysbiosis and neurodegeneration, diabetic, obesity and cancer have been postulated and in part also demonstrated [16–19]. * Correspondence: [email protected] 2 Department of Experimental Medicine, TOR, University of Rome Tor Vergata, Rome, Italy 3 School of Life Sciences, University of Nottingham, Nottingham, UK Full list of author information is available at the end of the article
Colorectal cancer (CRC) is directly linked to gut microbiota. CRC-enriched bacteria have been identified with faecal metagenomic approaches on patients with CRC [20, 21]. These include Parvimonas micra, Fusobacterium nucleatum, Bacteroides fragilis, Porphyromonas asaccharolytica, Thermanaerovibrio acidaminovorans, Prevotella intermedia and Alistipes finegoldii [22, 23]. They may serve as diagnostic markers of diseases; they may also direct on a better understanding of the CRC pathogenesis and may provide therapeutic strategies in the future. An important aspect that links dysbiosis and cancer pathogenesis is inflammation. Bacterial infection can indeed result in cancer. Gastric infection with Helicobacter pylori causes persistent inflammation and gastritis, resulting in a significa
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