Abstract
Establishing effective methods for preventing colorectal cancer by so-called “functional foods” is important because the global burden of colorectal cancer is increasing. Enterococcus faecalis strain EC-12 (EC-12), which belongs to the family of lactic acid bacteria, has been shown to exert pleiotropic effects, such as anti-allergy and anti-infectious effects, on mammalian cells. In the present study, we aimed to evaluate the preventive effects of heat-killed EC-12 on intestinal carcinogenesis. We fed 5-week-old male and female Apc mutant Min mice diets containing 50 or 100 ppm heat-killed EC-12 for 8 weeks. In the 50 ppm treated group, there was 4.3% decrease in the number of polyps in males vs. 30.9% in females, and significant reduction was only achieved in the proximal small intestine of female mice. A similar reduction was observed in the 100 ppm treated group. Moreover, heat-killed EC-12 tended to reduce the levels of c-Myc and cyclin D1 mRNA expression in intestinal polyps. Next, we confirmed that heat-killed EC-12 suppressed the transcriptional activity of the T-cell factor/lymphoid enhancer factor, a transcriptional factor involved in cyclin D1 mRNA expression in intestinal polyps. Our results suggest that heat-killed EC-12 very weakly suppresses intestinal polyp development in Min mice, in part by attenuating β-catenin signaling, and this implies that heat-killed EC-12 could be used as a “functional food”.
Highlights
Colorectal cancer (CRC) is the most common cancer and a major cause of cancer-related deaths in advanced countries, including Japan
We demonstrated that administration of heat-killed EC-12 weakly decreased intestinal tumorigenesis in Min mice, Apc-mutant mice that develop many intestinal polyps through activation of β-catenin signaling
We assessed the effectiveness of heat-killed EC-12 as a “functional food” for CRC prevention by evaluating its ability to suppress intestinal polyp development in Min mice
Summary
Colorectal cancer (CRC) is the most common cancer and a major cause of cancer-related deaths in advanced countries, including Japan. The global burden of CRC is estimated to increase by 60% to more than 2.2 million new cases and 1.1 million deaths by 2030 [1]. Establishing useful methods to prevent CRC is important. The development of sporadic CRC from normal mucosa takes an average of 10–20 years, thereby allowing us an opportunity for prevention. I.e., regular physical activity, smoking abstinence, and healthy nutrition, along with population screening methods for CRC check-ups, i.e., fecal occult blood testing and endoscopy, are popular CRC prevention methods. We need to consider alternative preventative strategies, such as cancer chemoprevention, including the use of so-called “functional foods”
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