TAILIEUCHUNG - Alteration in the subcellular location of the inhibitor of growth protein p33(ING1b) in estrogen receptor alpha positive breast carcinoma cells
ING1 has regulatory roles in the expression of genes associated with proliferation, apoptosis, and senescence. p33(ING1b) is the most widely expressed isoform of the gene. | Turkish Journal of Biology Turk J Biol (2017) 41: 105-112 © TÜBİTAK doi: Research Article Alteration in the subcellular location of the inhibitor of growth protein p33(ING1b) in estrogen receptor alpha positive breast carcinoma cells 1 2 3,4 5 2, İmge KUNTER , Emine KANDEMİŞ , Hani ALOTAİBİ , Tülay CANDA , Esra ERDAL BAĞRIYANIK * 1 Faculty of Pharmacy, Eastern Mediterranean University, Famagusta, North Cyprus via Mersin 10, Turkey 2 Department of Medical Biology and Genetics, Faculty of Medicine, Dokuz Eylül University, İzmir, Turkey 3 Department of Molecular Biology and Genetics, Faculty of Science, Bilkent University, Ankara, Turkey 4 Dokuz Eylül University, Advanced Biomedical Research Center, İzmir, Turkey 5 Department of Pathology, Faculty of Medicine, Dokuz Eylül University, İzmir, Turkey Received: Accepted/Published Online: Final Version: Abstract: ING1 has regulatory roles in the expression of genes associated with proliferation, apoptosis, and senescence. p33(ING1b) is the most widely expressed isoform of the gene. Downregulation of its nuclear expression is involved in differentiation and pathogenesis in invasive breast carcinoma. Yet the mechanism(s) by which p33 nuclear targeting is regulated remains unknown. In this study, we analyzed human invasive breast carcinoma tissue samples by immunostaining with p33 and correlating p33 location with the presence of ERα. Our findings show the expression of p33 protein in ERα-positive tumor samples was in the nucleus alone, while the expression was mainly in the cytoplasm in ERα-negative tumor samples. Examination of the localization of p33 in the nucleus and/or cytoplasm in several different cell lines demonstrated 17β-estradiol (E2) treatment causes dramatic compartmental shift in p33 protein from the cytoplasm to the nucleus in ERα-positive MDA-66 cells. No significant differences in ERα-negative MDA-MB-231
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