An investigation of the effect of culinary herbs on growth of colorectal cancer cells 'in vitro'

Jaksevicius, Andrius (2012) An investigation of the effect of culinary herbs on growth of colorectal cancer cells 'in vitro'. (MSc(R) thesis), Kingston University, .

Abstract

In the UK, colorectal cancer (CRC) is one of the most commonly diagnosed cancers and studies have identified COX-2 and the Wnt/ß-catenin signalling pathway, as key to the development of CRC. Culinary herbs, and their polyphenolie constituents, have been shown to inhibit COX-2 expression and inhibit the growth of cancer cells. However, few studies have investigated their effect onCRC cells. Thus the aim of this study was to investigate whether culinary herbs inhibit the growth of human CRC cells in vitro, and to determine the role of COX-2 expression and the Wnt /[beta]-catenin signalling pathway in this action. Aqueous and ethanol extracts of the culinary herbs bay leaf, parsley, rosemary sage and thyme were tested on CRC cell lines HT29 (COX-2 positive) and HCT116 (COX-2 negative). Growth inhibition studies revealed that with the exception of aqueous extracts of parsley all the other herb extracts inhibited the growth of HCT116 and HT29 cells in vitro. The IC50s varied based on the type of extract and cell type, suggesting that polyphenol composition within the extracts and cell type influenced the potency of the herbs. Western blotting showed that some herb extracts down-regulated COX-2 and unphosphorylated [beta]-catenin expression in the HT29 cell line, however, due to the poor quality of some of the blots, a more complete establishment of this effect was not possible. In conclusion, culinary herbs inhibit the growth of CRC cells in vitro however whether such an effect occurs in vivo requires further investigation. Some culinary herb extracts down-regulated COX-2 and unphosphorylated [beta]-catenin in HT29 cells, however, future studies are needed to confirm whether culinary herbs, and their constituent polyphenols, indeed modulate these two molecular targets as part of the prevention and/or treatment of CRC.

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