Abstract
An incorrect food regimen from childhood is suggested to negatively impact the gut microbiome composition leading to obesity and perhaps to colon rectal cancer (CRC) in adults. In this study, we show that the obesity and cancer gut microbiota share a characteristic microbial profile with a high colonization by mucin degraders species, such as Hafnia alvei and Akkermansia muciniphila. In addition, the species Clostridium bolteae, a bacterium associated with insulin resistance, dyslipidemia, and inflammation, has been associated with the presence of oncogenic Human Polyomaviruses (HPyVs). Merkel cell Polyomavirus (MCPyV) and BK Polyomavirus (BKPyV) were the most frequently oncogenic viruses recovered in the gut of both obese and tumor patients. Considering the high seroprevalence of HPyVs in childhood, their association with specific bacterial species deserve to be further investigated. Data from the present study highlight the presence of a similar microbiome pattern in CRC and obese subjects, suggesting that obese microbiome may represent an opportunity for tumorigenic/driver bacteria and viruses to trigger cell transformation.
Highlights
Colorectal cancer (CRC) is a major public health concern, as it is one of the leading causes of cancer deaths in the Western world [1]
We show that the obesity and cancer gut microbiota share a characteristic microbial profile with a high colonization by mucin degraders species, such as Hafnia alvei and Akkermansia muciniphila
Merkel cell Polyomavirus (MCPyV) and BK Polyomavirus (BKPyV) were the most frequently oncogenic viruses recovered in the gut of both obese and tumor patients
Summary
Colorectal cancer (CRC) is a major public health concern, as it is one of the leading causes of cancer deaths in the Western world [1]. CRC requires decades to clinically manifest, starting from the initial transformed intestinal crypt cells [2] This means that some risk factors could be traced back to the childhood and early adulthood. The increase in the CRC incidence is considered a consequence of the modern life-style and is associated with calorically excessive high-fat/low-fiber diet, consumption of refined products, lack of physical activity, and obesity [3,4]. This association seems to be stronger when childhood overweight persists into early adulthood than when the overweight disappears before early adulthood or develop after childhood [5]. The time of exposure to these metabolic changes, especially if present since childhood, may increase the chances for the development of CRC in adulthood
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