Research Papers:
Iodine stimulates estrogen receptor singling and its systemic level is increased in surgical patients due to topical absorption
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Shaohua He1, Bingchan Wang1, Xiyi Lu1, Suyu Miao1, Fengming Yang1, Theodore Zava2, Qiang Ding3, Shijiang Zhang4, Jiayin Liu5, David Zava2 and Yuenian Eric Shi1,6
1Departments of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
2ZRT Laboratory, Beaverton, Oregon, USA
3Departments of Surgery, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
4Departments of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
5Departments of Obstetrics and Gynecology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China
6State Key Laboratory of Reproductive medicine, Nanjing Medical University, Nanjing, China
Correspondence to:
Yuenian Eric Shi, email: [email protected]
Keywords: iodine, ER-α, breast cancer
Received: June 20, 2017 Accepted: July 26, 2017 Published: September 04, 2017
ABSTRACT
Iodine is crucial for thyroid hormone production. However, recent epidemiologic studies have shown that breast cancer patients have an elevated risk of developing thyroid cancer and vice versa. A notable finding in this study is that iodine stimulated the transcriptional activity of estrogen receptor-α (ER-α) in breast cancer cells. Iodine stimulated expression of several ER-α regulated gene including PS2, Cathepsin D, CyclinD1, and PR both in vitro and in nude mice, which is consistent with its stimulation of both anchorage-dependent and -independent growth of ER-α positive breast cancer cells and the effect to dampen tumor shrinkage of MCF-7 xenograft in ovariectomized nude mice. Analyses of clinical urine samples from breast cancer patients undergoing surgery demonstrated that urinary iodine levels were significantly higher than that in controls; and this increased level is due to the antiseptic use of iodine during breast surgery. The present study indicates that excess iodine intake may be an unfavorable factor in breast cancer by stimulation of ER-α transcriptional activity.