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Cyclooxygenase-2 expression during immortalization and breast cancer progression
Xiangshan Zhao1, Monica Goswami, Nidhi Pokhriyal
1Division of Cancer Biology, Department of Medicine, Evanston Northwestern Healthcare Research Institute and Feinberg School of Medicine, Evanston, IL, USA.
Cancer Research
|January 18, 2008
Summary
Cyclooxygenase 2 (COX-2) is not a reliable marker for identifying breast cancer precursor cells. Its expression decreases during tumor progression and does not impact cell growth or oncogenic behavior.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Identifying molecular changes in premalignant human mammary epithelial cells (hMEC) is crucial for understanding breast cancer development.
- Previous research suggested cyclooxygenase 2 (COX-2) expression could mark precursor cells for breast cancer.
Purpose of the Study:
- To investigate the role of COX-2 expression in breast cancer precursor cells and its association with tumor progression.
- To determine if COX-2 expression influences the transformation and oncogenic behavior of hMEC.
Main Methods:
- Analyzed COX-2 expression in preselection and postselection hMEC, immortalized cells, breast cancer cell lines, and clinical specimens.
- Utilized small interfering RNA to down-regulate COX-2 in cells.
- Assessed the impact of COX-2 down-regulation on cell proliferation, anchorage-independent growth, migration, and invasion.
Main Results:
- COX-2 levels were similar in preselection and postselection hMEC but decreased significantly upon immortalization.
- Breast cancer cell lines and tumor specimens exhibited lower COX-2 expression compared to normal hMEC.
- Down-regulating COX-2 did not affect hMEC proliferation, growth, migration, or invasion.
Conclusions:
- COX-2 overexpression does not appear to identify breast cancer precursor cells or confer a transformation advantage.
- COX-2 inhibition does not impact hMEC growth or oncogenic potential under the studied conditions.
- COX-2 expression is downregulated during breast cancer progression from normal epithelial cells to invasive carcinoma.
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