Prognosis of Colorectal Cancer in Inflammatory Bowel Disease: Data from a State Registry

Ullman, Thomas; Itzkowitz, Steven H.

doi:10.1007/s10620-017-4557-3

Cited by 1 publication

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“…Colorectal cancer is a multifactorial disease involving genetic, environmental and lifestyle risk factors. In the development of colorectal cancer, chronic inflammation has been identified as a key predisposing factor ( 20 , 21 ). The inflammatory state of the colon can strongly influence the process of colorectal cancer, and subtle inflammation in otherwise healthy colonic tissues may cause the conversion of a healthy colon into a dysplastic colon, as well ( 22 ).…”

Section: Discussionmentioning

confidence: 99%

Effects of compound K, an enteric microbiome metabolite of ginseng, in the treatment of inflammation associated colon cancer

et al. 2018

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Ginsenoside Rb1, a major component of different ginseng species, can be bioconverted into compound K by gut microbiota, and the latter possess much stronger cancer chemopreventive potential. However, while the initiation and progression of colorectal cancer is closely associated with gut inflammation, to date, the effects of compound K on inflammation-linked cancer chemoprevention have not been reported. In the present study, liquid chromatography quadrupole time-of-flight mass spectrometry analysis was applied to evaluate the biotransformation of Rb1 in American ginseng by human enteric microflora. The in vitro inhibitory effects of Rb1 and compound K were compared using the HCT-116 and HT-19 human colorectal cancer cell lines by a MTS assay. Cell cycle and cell apoptosis were assayed using flow cytometry. Using ELISA, the anti-inflammatory effects of Rb1 and compound K were compared for their inhibition of interleukin-8 secretion in HT-29 cells, induced by lipopolysaccharide. The results revealed that compound K is the major intestinal microbiome metabolite of Rb1. When compared with Rb1, compound K had significantly stronger anti-proliferative effects in HCT-116 and HT-29 cell lines (P<0.01). Compound K significantly arrested HCT-116 and HT-29 cells in the G1 phase, and induced cell apoptosis (P<0.01). By contrast, Rb1 did not markedly influence the cell cycle or apoptosis. Furthermore, compound K exerted significant anti-inflammatory effects even at low concentrations (P<0.05), while Rb1 did not have any distinct effects. The data obtained from the present study demonstrated that compound K, an intestinal microbiome metabolite of Rb1, may have a potential clinical value in the prevention of inflammatory-associated colorectal cancer.

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Section: Discussionmentioning

confidence: 99%