We found a match
Your institution may have rights to this item. Sign in to continue.
- Title
Tunicamycin significantly reduces the MCF-7 human breast cancer cell proliferation.
- Authors
Trujillo, Uldaeliz; Banerjee, Dipak K.
- Abstract
Breast cancer is the most frequently diagnosed cancer in women, accounting for one out of every eight women. The etiology of the disease is complex and requires neovascularization for the growth of a malignant tumor. Our laboratory has observed recently that tunicamycin, (a) an antibiotic, (b) a glucosamine-containing pyrimidine nucleoside, and (c) a protein N-glycosylation inhibitor reduces angiogenesis significantly. This was due to an induction of unfolded protein response-mediated cell cycle arrest and apoptosis. The objective of our present study is to test the hypothesis that tunicamyin inhibits MCF-7 cell proliferation. MCF-7 cells ware synchronized by serum deprivation for 48 hours, and treated with tunicamycin (0-10 µg/ml) for 24 hours. The cell morphology was monitored by light microscopy. The cell growth was reduced only 20-30% at 0.1 µg/ml and 1.0 µg/ml of tunicamycin, respectively but the inhibition was >70% at 10 µg/ml of tunicamycin. There was no indication of the cell cycle arrest. Total Bcl-2 expression was increased in the presence of 10 µg/ml and 0.1 pg/ml of tunicamycin as well as at "zero time". Bak expression was not detected but a high level expression of Bax, Bad and p53 was detected at low tunicamycin concentration. There was no detectable expression of either caspase 3 or 9. Therefore, we conclude that tunicamycin-mediated MCF-7 cells death may not be due to an induction apoptosis. Flow cytometric evaluation of the cell cycle also supports such conclusion.
- Subjects
TUNICAMYCIN; CANCER cell growth regulation; CANCER cell proliferation; BREAST cancer; CELL proliferation; CELL cycle; APOPTOSIS; CANCER in women
- Publication
FASEB Journal, 2007, Vol 21, Issue 6, pA1009
- ISSN
0892-6638
- Publication type
Article
- DOI
10.1096/fasebj.21.6.a1009-d