METHIONINE CYTOTOXICITY IN THE HUMAN BREAST CANCER CELL LINE MCF-7

• Published in: In vitro cellular & developmental biology. Animal 2003-03, Vol.39 (3), p.117-119
• Main Authors: KIM, HYUNG H, PARK, CHUNG S
• Format: Article
• Language: English
• Subjects: Breast cancer; Breast Neoplasms - pathology; Cancer; Cell cycle; Cell Division - drug effects; Cell growth; Cell Line, Tumor; Cell lines; cell proliferation; Cell Survival - drug effects; Cultured cells; Diet; Female; Humans; mammary cancer; MCF-7; methionine; Methionine - toxicity; p53; RNA; RNA, Ribosomal, 28S - drug effects; RNA, Ribosomal, 28S - genetics; Tumor cell line; Tumors
• ISSN: 1071-2690; 1543-706X; 1543-706X
• DOI: 10.1290/1543-706X(2003)039<0117:MCITHB>2.0.CO;2

Among the first nutrients to be linked to cancer were methyl group containing nutrients including methionine. Methionine and its metabolic derivatives are essential components in several indispensable biological reactions including protein synthesis, polyamine synthesis, and many transmethylation reactions. The purpose of this study was to determine the extent to which methionine excess affects the proliferation and gene expression of the human breast cancer cell line MCF-7. Cells were first grown in control medium; the medium was then replaced with either control or methionine-supplemented treatment media. We found that 5 and 10 g/L methionine significantly suppressed cell growth on day 1, and no further growth was detected after 3 d of treatment. Cell proliferation in the methionine treated group was significantly lower than that of the control group. Northern analysis revealed that expression of p53 in methionine-treated MCF-7 cells was approximately 70% lower than that of control cells. p53 is a key cell cycle regulatory protein that has been implicated in tumorigenesis and cancer progression. Alteration of the p53 tumor suppressor gene is the most common genetic change found in a wide variety of malignancies, including cancer. This study shows that excess methionine (5 g/L) inhibited proliferation of MCF-7 breast cancer cells, and down regulation of p53 is correlated with this inhibition. These findings may aid in the development of nutritional strategies for breast cancer therapy.