Abstract
PurposeWatercress is a rich source of phytochemicals with anticancer potential, including phenethyl isothiocyanate (PEITC). We examined the potential for watercress extracts and PEITC to increase the DNA damage caused by ionising radiation (IR) in breast cancer cells and to be protective against radiation-induced collateral damage in healthy breast cells. The metabolic events that mediate such responses were explored using metabolic profiling.Methods1H nuclear magnetic resonance spectroscopy-based metabolic profiling was coupled with DNA damage-related assays (cell cycle, Comet assay, viability assays) to profile the comparative effects of watercress and PEITC in MCF-7 breast cancer cells and MCF-10A non-tumorigenic breast cells with and without exposure to IR.ResultsBoth the watercress extract and PEITC-modulated biosynthetic pathways of lipid and protein synthesis and resulted in changes in cellular bioenergetics. Disruptions to the redox balance occurred with both treatments in the two cell lines, characterised by shifts in the abundance of glutathione. PEITC enhanced the sensitivity of the breast cancer cells to IR increasing the effectiveness of the cancer-killing process. In contrast, watercress-protected non-tumorigenic breast cells from radiation-induced damage. These effects were driven by changes in the cellular content of the antioxidant glutathione following exposure to PEITC and other phytochemicals in watercress.ConclusionThese findings support the potential prophylactic impact of watercress during radiotherapy. Extracted compounds from watercress and PEITC differentially modulate cellular metabolism collectively enhancing the therapeutic outcomes of radiotherapy.
Highlights
Breast cancer is a leading cause of cancer-related mortalities globally
Impact on cell proliferation of increasing doses of the crude watercress extract and phenethyl isothiocyanate (PEITC) was assessed in MCF-7 and MCF-10A cells
The combination of PEITC or watercress treatment and ionising radiation (IR) on the overall metabolic activity of the cells was assessed using the MTT assay as a proxy of viable, metabolically active cells
Summary
Breast cancer is a leading cause of cancer-related mortalities globally. Over 266,000 new breast cancer cases are projected to occur solely in the United States in 2018 accounting for over 40,000 deaths [1]. European Journal of Nutrition (2019) 58:2377–2391 treatment modality for breast cancer patients. This approach uses the fractionated delivery of high-energy X-ray beams to generate highly reactive free radicals in target tumour tissue. This causes DNA damage via lipid peroxidation or oxidative cellular respiration. Radiation-induced damage activates several signal transduction pathways whose primary role is to detect genomic injury leading to cell cycle arrest and DNA repair. Radiotherapy causes damage in healthy cells and can potentially trigger new cancer-initiating DNA mutations in local tissue. Therapeutic selectivity is, a vital issue in cancer therapy, and an ideal anticancer agent should be toxic to cancerous cells but exert minimal toxicity in healthy cells
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