Does colorectal cancer significantly influence the assembly of gut microbial communities?

Colorectal cancer (CRC) is the third commonest malignant tumor. Previous studies have revealed that the composition change of the human gut microbiome, measured by community diversity, is associated with the progression of CRC. However, a further question, whether or not the mechanism of community assembly and diversity maintenance of the gut microbiome is influenced by CRC has not been addressed. To address this question, we applied Hubbell's neutral theory for biodiversity to reanalyze the dataset from Wang et al.'s (2012) study of the gut microbiome sampled from 46 CRC patients and 56 healthy individuals. Our reanalysis presents two important findings. Firstly, our analysis demonstrated that only around 4% (4/102) samples (in total of both the CRC and control groups) have their species abundance distribution (SAD) satisfied the prediction of the neutral theory null model. No significant difference in the number of the samples satisfying the neutral null model was detected between the healthy individuals and CRC patients, suggesting that the nature or mechanism of community assembly and diversity maintenance of the gut microbiome is not significantly influenced by CRC. That is, the stochasticity of survival, reproduction and migration of gut microbes, as implied by the neutral theory model, does not play a significant role in shaping the community assembly and diversity maintenance. We further infer that the alternative hypothesis to the neutral null model, i.e., the deterministic niche differentiations should be the driving forces that shape the assembly and diversity maintenance of the gut microbiome in both the healthy individuals and CRC patients. Secondly, although CRC does not seem to influence the nature of community assembly, we postulate that it may indirectly influence the outcome (i.e., the community composition as measured by community diversity) of the community assembly, possibly by influencing niche differentiations. This postulation is supported by our second finding: the diversity of the gut microbiome in CRC patients is significantly lower than that in the healthy individuals as demonstrated by the fundamental diversity parameter (θ) of the neutral theory model. This second finding offers an independent confirmation of the relationship between the CRC disease and diversity of the gut microbiome, about which existing studies have presented conflicting evidences. Finally, we suggest that hybrid modeling which integrates both the neutral and niche theories should be explored in future studies to further understanding of the CRC influence on the human gut microbiome.