Abstract
Colorectal cancer is an increasingly significant cause of mortality whose risk is linked to diet and inversely correlated with cruciferous vegetable consumption. This is likely to be partly attributable to the isothiocyanates derived from eating these vegetables, such as sulforaphane, which is extensively characterised for cytoprotective and tumour-suppressing activities. However, its bioactivities are likely to extend in complexity beyond those currently known; further insight into these bioactivities could aid the development of sulforaphane-based chemopreventive or chemotherapeutic strategies. Evidence suggests that sulforaphane modulates the expression of microRNAs, many of which are known to regulate genes involved at various stages of colorectal carcinogenesis. Based upon existing knowledge, there exist many plausible mechanisms by which sulforaphane may regulate microRNAs. Thus, there is a strong case for the further investigation of the roles of microRNAs in the anti-cancer effects of sulforaphane. There are several different types of approach to the wide-scale profiling of microRNA differential expression. Array-based methods may involve the use of RT-qPCR or complementary hybridisation probe chips, and tend to be relatively fast and economical. Cloning and deep sequencing approaches are more expensive and labour-intensive, but are worth considering where viable, for their greater sensitivity and ability to detect novel microRNAs.
Highlights
Colorectal cancer is an increasingly significant cause of mortality whose risk is linked to diet and inversely correlated with cruciferous vegetable consumption
Two cell lines—normal derived colon mucosa 460 (NCM460) and normal derived colon mucosa 356 (NCM356)—were used, and TaqMan Low Density qPCR Arrays were used to profile the differential expression of 754 human miRNAs following 48 h SFN treatment [44]
Colorectal cancer poses an increasingly important health burden globally, with apparent links to diet that are unsurprising, given the liability of colorectum to be exposed to ingested compounds and products of the gut microbiota
Summary
Colorectal cancer is a major and increasingly common cause of morbidity and premature death. In 2015, 774,000 mortalities were directly attributable to colorectal cancer—a figure 58% higher than in 1990 [2] It is rare for tangible symptoms of colorectal cancer to present until it has already progressed to an advanced (usually terminal) stage, at which currently available treatments are unable to provide a cure [3]. There is compelling evidence to suggest that commonly associated dietary and lifestyle changes have a significant impact upon the development of colorectal cancer [5]. One’s risk of developing colorectal cancer is believed to be increased by obesity and a high intake of red meat and/or alcohol and reduced by a fibre-rich diet abundant in fruits and vegetables and a physically active lifestyle, according to Nutrients 2017, 9, 902; doi:10.3390/nu9080902 www.mdpi.com/journal/nutrients. The apparently protective effects of diets rich in plant-based foods are believed to be largely attributable to the phytochemicals found in them, many families of which have been studied regarding their direct biological (often cytoprotective) activity—both in vitro and in vivo—since the middle of the twentieth century
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