9 36. Kahn, S. E., D’Alessio, D. A., Schwartz, M. W., Fujimoto, W. Y., Ensinck, J. W., Taborsky, G. J., Jr., and Porte, D., Jr. (1990) Evidence of cosecretion of islet amyloid polypeptide and insulin by beta-cells. Diabetes 39,
INTERNATIONAL JOURNAL OF ONCOLOGY 44: 1365-1375,-D-glucan inhibits endocrine-resistant breast cancer cell proliferation and alters gene expressionZAINAB M.T. JAFAAR1*, LACEY M. LITCHFIELD2*, MARGARITA M. IVANOVA2*, BRANDIE N. RADDE2, NUMAN AL-RAYYAN2,3 and CAROLYN M. KLINGECenter of Biotechnology, Agricultural Study Directorate, Ministry of Science and Technology, Baghdad, Iraq; two Department of Biochemistry and Molecular Biology, Center for Genetics and Molecular Medicine, University of Louisville College of Medicine, Louisville, KY 40292, USA Received November 22, 2013; Accepted December 30, 2013 DOI: 10.3892/ijo.2014.Abstract. Endocrine therapies have already been effectively applied for breast cancer sufferers with estrogen receptor (ER) optimistic tumors, but 40 of sufferers relapse because of endocrine resistance. -glucans are components of plant cell walls which have immunomodulatory and anticancer activity. The objective of this study was to examine the activity of -D-glucan, purified from barley, in endocrine-sensitive MCF-7 versus endocrine-resistant LCC9 and LY2 breast cancer cells. -D-glucan dissolved in DMSO but not water inhibited MCF-7 cell proliferation within a concentrationdependent manner as measured by BrdU incorporation with an IC50 of 164?2 /ml. -D-glucan dissolved in DMSO inhibited tamoxifen/endocrine-resistant LCC9 and LY2 cell proliferation with IC50 values of 4.six?.three and 24.two?.4 /ml, respectively. MCF-10A typical breast epithelial cells showed a higher IC50 464 /ml and also the proliferation of MDA-MB231 triple unfavorable breast cancer cells was not inhibited by -D-glucan. Concentration-dependent increases inside the BAX/ BCL2 ratio and cell death with -D-glucan were observed in MCF-7 and LCC9 cells.SM-102 site PCR array analysis revealed changes in gene expression in response to 24-h therapy with 10 or 50 /ml -D-glucan that have been different amongst MCF-7 and LCC9 cells at the same time as variations in basal gene expression among the two cell lines. Pick results have been confirmed byquantitative real-time PCR demonstrating that -D-glucan increased RASSF1 expression in MCF-7 cells and IGFBP3, CTNNB1 and ER transcript expression in LCC9 cells.Formula of 131180-63-7 Our information indicate that -D-glucan regulates breast cancer-relevant gene expression and may well be useful for inhibiting endocrineresistant breast cancer cell proliferation.PMID:23537004 Introduction Acquired resistance to antiestrogen or aromatase inhibitor therapy affects 40-50 of patients whose breast tumors are estrogen receptor (ER)-positive (1). Various mechanisms contribute to endocrine resistance and new therapies are needed to stop endocrine resistance and treat these individuals (2). (1-3)-D-glucans are diverse polysaccharides derived from plant cell walls composed of D-glucose monomers linked by (1-3)-glycosidic bonds. The activities of -glucans have been studied in vivo and in vitro (three). When ingested in plant components, -glucans are absorbed within the modest intestine and taken up by macrophages. -glucans are considered to be `biological response modifiers’ given that they exhibit immunomodulatory, wound-healing, antiviral, antibacterial, anti-coagulatory and antitumoral activities (four). Because of their size, -glucans function by binding to cell surface receptors (five). -glucans act on a number of immune rece.