In healthy hosts, trillions of microbes colonise the gut and oral cavity in a well-balanced state, maintaining a mutually beneficial relationship. Loss of this balance, termed dysbiosis, is strongly implicated in the pathogenesis of colorectal cancer (CRC). However, the roles of microbiota and dysbiosis in CRC treatment remain poorly understood. Recent studies suggest that the gut microbiota has the ability to affect the host response to chemotherapeutic agents by enhancing drug efficacy, promoting chemoresistance and mediating chemotherapy-induced toxicity and side effects via a variety of mechanisms. Several other studies have also proposed manipulation of the microbiota to optimise CRC treatment. In this review, we summarise the current advancement of knowledge on how microbiota and CRC treatments interact with each other and how this interaction may shed some light on the development of personalised microbiota manipulations that improve CRC treatment outcomes.
Alteration of the gut virome has been associated with colorectal cancer (CRC); however, when and how the alteration takes place has not been studied. Here, we employ a longitudinal study in mice to characterize the gut virome alteration in azoxymethane (AOM)-induced colorectal neoplasia and identify important viruses associated with tumor growth. The number and size of the tumors increased as the mice aged in the AOM treated group, as compared to the control group. Tumors were first observed in the AOM group at week 12. We observed a significantly lower alpha diversity and shift in viral profile when tumors first appeared. In addition, we identified novel viruses from the genera Brunovirus, Hpunavirus that are positively associated with tumor growth and enriched at a late time point in AOM group, whereas members from Lubbockvirus show a negative correlation with tumor growth. Moreover, network analysis revealed two clusters of viruses in the AOM virome, a group that is positively correlated with tumor growth and another that is negatively correlated with tumor growth, all of which are bacteriophages. Our findings suggest that the gut virome changes along with tumor formation and provides strong evidence of a potential role for bacteriophage in the development of colorectal neoplasia.
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