Carcinogen 7,12-dimethylbenz[a]anthracene-induced mammary tumorigenesis is accelerated in Smad3 heterozygous mice compared to Smad3 wild type mice
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Zhengxue Liu1,2,3,8, Tanima Kundu-Roy1,2,3, Isao Matsuura1,2,3,6, Guannan Wang1,2,3, Yong Lin4, You-Rong Lou2, Nicola J. Barnard5, Xiao-Fan Wang7, Mou-Tuan Huang2, Nanjoo Suh2,3 and Fang Liu1,2,3
1 Center for Advanced Biotechnology and Medicine, Rutgers, The State University of New Jersey, Piscataway, NJ, USA
2 Susan Lehman Cullman Laboratory for Cancer Research, Department of Chemical Biology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ, USA
3 Rutgers Cancer Institute of New Jersey, New Brunswick, NJ, USA
4 Department of Biostatistics, School of Public Health, Rutgers, The State University of New Jersey, Piscataway, NJ, USA
5 Department of Pathology, Rutgers Robert Wood Johnson Medical School, Piscataway, NJ, USA
6 Division of Molecular Genomics and Medicine, National Health Research Institutes, Zhunan, Miaoli County, Taiwan
7 Department of Pharmacology and Cancer Biology, Duke University Medical Center, Durham, NC, USA
8 College of Life Science & Engineering, Chongqing Three Gorges University, Chongqing, China
Fang Liu, email:
Keywords: Smad3, TGF-ß, DMBA, carcinogenesis, breast cancer
Received: October 15, 2015 Accepted: August 01, 2016 Published: August 30, 2016
Previous studies based on cell culture and xenograft animal models suggest that Smad3 has tumor suppressor function for breast cancer during early stages of tumorigenesis. In this report, we show that DMBA (7,12-dimethylbenz[a]anthracene), a chemical carcinogen, induces mammary tumor formation at a significantly higher frequency in the Smad3 heterozygous mice than in the Smad3 wild type mice. This is the first genetic evidence showing that Smad3 inhibits mammary tumor formation in a mouse model. Our findings support the notion that Smad3 has important tumor suppressor function for breast cancer.
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