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A benzoxazine derivative specifically inhibits
cell cycle progression in p53-wild type pulmonary adenocarcinoma cells |
| Hua SU1,Ling SU1,Qiuxia HE2,Jing ZHAO2,Shangli ZHANG2,Junying MIAO2,Baoxiang ZHAO3, |
| 1.Institute of Developmental
Biology, School of Life Science, Shandong University, Jinan 250100,
China; 2.Institute of Developmental
Biology, School of Life Science, Shandong University, Jinan 250100,
China；The key Laboratory of
Experimental Teratology Ministry of Education, Jinan 250012, China; 3.Institute of Organic
Chemistry, School of Chemistry and Chemical Engineering, Shandong
University, Jinan 250100, China; |
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Abstract A fundamental aspect of cancer development is cancer cell proliferation. Seeking for chemical agents that can interfere with cancer cell growth has been of great interest over the years. In our study, we found that a benzoxazine derivative, (6-tert-butyl-3,4-dihydro-2H-benzo[b][1,4]oxazin-3-yl) methanol (TBM), could inhibit cell growth and caused significant cell cycle arrest in pulmonary adenocarcinoma A549 and H460 cells with wild-type p53, while not affecting the cell cycle distribution in p53-deleted H1299 lung adenocarcinoma cells. Since P53 plays an important role in regulating cell cycle progression, we analyzed the protein level of p53 by Western blot, and detected a significant elevation of p53 level after TBM treatment in A549 and H460 cells. The data suggested that TBM might specifically inhibit the proliferation of p53 wild-type lung adenocarcinoma cells through a p53-dependent cell cycle control pathway. More interestingly, results indicated that TBM might serve as a useful tool for studying the molecular mechanisms of lung cancer cell growth and cell cycle control, especially for the biologic process regulated by P53.
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| Keywords
(6-tert-butyl-3,4-dihydro-2H-benzo[b][1,4]oxazin-3-yl) methanol
lung adenocarcinoma cells
cell cycle arrest
p53
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Issue Date: 01 April 2010
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