Premium
Human breast cancer (MCF‐7) cells are less sensitive to angiogenesis inhibitor tunicamycin
Author(s) -
Rodriguez Uldaeliz Trujillo,
Colon Jonathan Caldera,
Sanchez Aurymar,
Banerjee Dipak K
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a55-d
Subject(s) - tunicamycin , angiogenesis , cancer cell , cancer research , unfolded protein response , apoptosis , mcf 7 , chemistry , cancer , biology , immunology , medicine , biochemistry , human breast
Breast cancer is the most frequently diagnosed cancer in women, accounting for one out of every three cancer diagnosis. The etiology of breast cancer is complex, but the continued growth of a malignant tumor beyond a certain critical size requires neovascularization (i.e., angiogenesis). Our laboratory has observed recently that tunicamycin (an antibiotic) inhibits angiogenesis by arresting the cells in G1 and inducing apoptosis. Tunicamycin, a glucosamine‐containing pyrimidine nucleoside and inhibits N‐acetylglucosaminyl‐1 phosphate transferase (GPT) activity in the endoplasmic reticulum (ER). When treated with tunicamycin dolichol‐linked oligosaccharide Glc 3 Man 9 GlcNAC 2 ‐PP‐Dol (LLO) was not synthesized and the asparagine‐linked (N‐linked) glycoproteins were not glycosylated in capillary endothelial cells. This developed ER stress, and induced unfolded protein response (UPR)‐mediated apoptosis. The objective of the present study is to address that tunicamycin would be equally effective against the breast cancer cells growth and proliferation. To test the hypothesis we have exposed a synchronized population of MCF‐7 cells with tunicamycin (0–10 μg/ml). After every 24 hours the cell morphology was monitored by light microscopy. Cells were counted in a hemocytometer and processed for flow cytometry to analyze the cell cycle. We concluded that tunicamycin inhibited the MCF‐7 cells proliferation and induced apoptotic cell death at a much higher concentration. Supported in part by grants from MBRS‐RISE Program R25‐GM61838, DAMD17‐03‐1‐0754, and U54‐CA096297.