【摘 要】
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Previous studies have demonstrated that the persistent exposure of human bronchial epithelial cells to nicotine (Nic) through nicotinic acetylcholine receptors increases cyclin D1 promoter activity an
【机 构】
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Superintendent, Clinical Professor Taipei Medical University Hospital Taipei Medical University Taiw
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Previous studies have demonstrated that the persistent exposure of human bronchial epithelial cells to nicotine (Nic) through nicotinic acetylcholine receptors increases cyclin D1 promoter activity and protein expression.The main purpose of this study was to elucidate the carcinogenic role of cyclin D3, which is involved in breast tumorigenesis when induced by Nic.Real-time PCR analysis revealed that cyclin D3 is highly expressed at the mRNA level in surgically dissected breast tumor tissue compared to the surrounding normal tissue (Tumor/Normal fold ratio =17.93, n =74).
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