• probiotics and colorectal cancer
  • Hossein Zahmatkesh Zakariaee,1,*
    1. Faculty of Basic Sciences-Lahijan Branch-Lahijan/Iran


  • Introduction: The human body contains more than 100 trillion microbes, most of which are hosted in the gut, although there are different communities residing in a vast range of body niches. This population is called the microbiome and comprises a wide variety of microorganisms, including archaea, viruses and fungi, although anaerobic bacteria is the most studied group since they are the most abundant. These microbial communities are acquired at birth and are essential for maintaining body homeostasis. The interaction between the host and the microbiome is dynamic and controlled by a huge number of genetic and environmental factors, such as age, geography, alcohol or drug intake and diet. although intestinal microbiota have been shown to be individual and variable over time, only two predominant phyla, namely Firmicutes and Bacteroidetes, comprise over 90% of all endogenous bacteria present in healthy adults. Other members of the normal colonic microbiome include Eubacterium, Bifidobacterium, Fusobacterium, Lactobacilli, Enterococci, Streptococci or Enterobacteriaceae.
  • Methods: Dysbiosis and Colorectal Cancer: Breaking the Mutualism Although it is not yet clear how dysbiosis could induce colonic carcinogenesis, chronic inflammation appears to be the main mechanism. This hypothesis is supported by the fact that many types of cancer are caused by chronic inflammation. For example, inflammatory bowel diseases (IBD) are linked to an increased risk of colon cancer. The first stages of these diseases involve an alteration to the normal flora, which results in activation of the immune system, thus giving rise to the inflammation that characterizes IBD. As IBD patients have a higher probability of suffering CRC, and dysbiosis has been observed in some cases, it is possible to assume that IBD-related CRC is driven by a previous dysbiosis stage. As a result, the microbiome has started to be considered one of the prime suspects responsible for the onset and/or evolution of colonic carcinogenesis. This research field is based on the differences found in microbial signature between CRC patients and healthy populations. Indeed, next-generation sequencing methods based on 16s rRNA have revealed an enrichment in proinflammatory bacteria, such as Fusobacterium, which is also overrepresented in other diseases (for example IBD), as well as a lower abundance of butyrate producers, such as protective bifidobacteria.
  • Results: Potential mechanisms of probiotic action in CRC chemoprevention Adhesion of probiotics and competitive exclusion of pathogenic intestinal flora Alteration of intestinal microflora enzyme activity Reduction of carcinogenic secondary bile acids Binding of carcinogens and mutagens Chemopreventive role of short chain fatty acids
  • Conclusion: In conclusion, there is a convincing body of evidence suggesting various potential mechanisms of action of probiotics in CRC prevention. It is clear that the chemopreventive effects of probiotics are dependent on the strain of the microorganism. Emerging data suggest viability may not be a prerequisite for probiotics to exert its anti-CRC activity. Synbiotics is likely to be more effective than either prebiotics or probiotics alone, as indicated by the growing body of data. More in vivo, especially human studies are warranted to further elucidate and confirm the potential chemopreventive role of probiotics (viable and non-viable), prebiotics and synbiotics in CRC.
  • Keywords: Probiotics; Colon; colorectal carcinoma; microbiota; cancer