PMID- 9566703 OWN - NLM STAT- MEDLINE DCOM- 19980508 LR - 20190720 IS - 0304-3835 (Print) IS - 0304-3835 (Linking) VI - 125 IP - 1-2 DP - 1998 Mar 13 TI - Inhibitory effect of selenomethionine on the growth of three selected human tumor cell lines. PG - 103-10 AB - Selenium supplementation has been shown for many years to work as an anticarcinogenic agent both in epidemiology and in in vitro studies. Selenium supplementation has recently been shown to decrease total cancer incidence. However, the mechanism of action of selenium as an anticarcinogenic agent has yet to be elucidated. Selenomethionine was the predominant form of selenium in the dietary supplement in the study by Clark et al. (Clark, L.C., Combs, G.F., Turnbull, W.B., Slate, E.H., Chalker, D.K., Chow, J., Davis, L.S., Glover, R.A., Graham, G.F., Gross, E.G., Krongrad, A., Lesher, J.L., Park, H.K., Sanders, B.B., Smith, C.L., Taylor, J.R. and The Nutritional Prevention of Cancer Study Group (1996) Effects of selenium supplementation for cancer prevention in patients with carcinoma of the skin: a randomized controlled trial. J. Am. Med. Assoc., 276 (24), 1957-1963) and therefore we evaluated the growth inhibitory effects of selenomethionine against human tumor cells. Selenomethionine was tested against each of three human tumor cell lines (MCF-7/S breast carcinoma, DU-145 prostate cancer cells and UACC-375 melanoma) and against normal human diploid fibroblasts. All cell lines demonstrated a dose-dependent manner of growth inhibition by selenomethionine. Selenomethionine inhibited the growth of all of the human tumor cell lines in the micromolar (microM) range (ranging from 45 to 130 microM) while growth inhibition of normal diploid fibroblasts required 1 mM selenomethionine, approximately 1000-fold higher than for the cancer cell lines. In short, normal diploid fibroblasts were less sensitive than the cancer cell lines to the growth inhibitory effects of selenomethionine. Furthermore, we show that selenomethionine administration to these cancer cell lines results in apoptotic cell death and aberrant mitoses. These results demonstrate the differential sensitivity of tumor cells and normal cells to selenomethionine. FAU - Redman, C AU - Redman C AD - Pharmacology/Toxicology Department, The University of Arizona, Tucson 85724, USA. FAU - Scott, J A AU - Scott JA FAU - Baines, A T AU - Baines AT FAU - Basye, J L AU - Basye JL FAU - Clark, L C AU - Clark LC FAU - Calley, C AU - Calley C FAU - Roe, D AU - Roe D FAU - Payne, C M AU - Payne CM FAU - Nelson, M A AU - Nelson MA LA - eng GR - CA41108-MIS/CA/NCI NIH HHS/United States GR - R29 CA 70145-01/CA/NCI NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - Ireland TA - Cancer Lett JT - Cancer letters JID - 7600053 RN - 0 (Antineoplastic Agents) RN - 964MRK2PEL (Selenomethionine) SB - IM MH - Antineoplastic Agents/*pharmacology MH - Breast Neoplasms/pathology MH - Dose-Response Relationship, Drug MH - Female MH - Humans MH - Male MH - Melanoma/pathology MH - Prostatic Neoplasms/pathology MH - Selenomethionine/*pharmacology MH - Tumor Cells, Cultured EDAT- 1998/05/05 00:00 MHDA- 1998/05/05 00:01 CRDT- 1998/05/05 00:00 PHST- 1998/05/05 00:00 [pubmed] PHST- 1998/05/05 00:01 [medline] PHST- 1998/05/05 00:00 [entrez] AID - S0304-3835(97)00497-7 [pii] AID - 10.1016/s0304-3835(97)00497-7 [doi] PST - ppublish SO - Cancer Lett. 1998 Mar 13;125(1-2):103-10. doi: 10.1016/s0304-3835(97)00497-7.