Research article
Altered serotonin physiology in human breast cancers favors paradoxical growth and cell survival
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* Corresponding author: Nelson D Horseman nelson.horseman@uc.edu
1 Department of Molecular and Cellular Physiology, University of Cincinnati, 231 Albert Sabin Way, Cincinnati, OH, 45267-0576, USA
2 Systems Biology and Physiology Program, University of Cincinnati, 231 Albert Sabin Way, Cincinnati, OH, 45267-0576, USA
3 James L. Winkle College of Pharmacy, University of Cincinnati, 3225 Eden Ave, Cincinnati, OH, 45267-0004, USA
4 Current address: Tufts Center for Regenerative and Developmental Biology and Biology Department, Tufts University, 200 Boston Ave, Medford, MA, 02155, USA
Breast Cancer Research 2009, 11:R81 doi:10.1186/bcr2448
Published: 10 November 2009Additional files
Additional file 1:
PDF document containing Table S1, primers used for detecting 5-HT receptors; Figure S1, which compares SERT protein levels between non-transformed and breast cancer cells; Figure S2 is TPH1 staining intensity key for scoring tissue microarray sections; Figure S3 represents changes in TPH1 signal in human breast tumors; Figure S4 represents differences in 5-HT receptor isoform gene expression between non-transformed (pHMECs and MCF10A) and breast cancer cells (MCF7, MDA-MB-231 and T47D; Figure S5 depicts 5-HT inhibition of cell growth in non-transformed mammary epithelial cells; and Figure S6 shows that the 5-HT effect on cell proliferation at 36 h is not influenced by cell death.
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