Cytotoxicity of I-125-oestrogen decay in non-oestrogen receptor-expressinghuman breast cancer cells, MDA-231 and oestrogen receptor-expressing MCF-7cells

Citation
Ls. Yasui et al., Cytotoxicity of I-125-oestrogen decay in non-oestrogen receptor-expressinghuman breast cancer cells, MDA-231 and oestrogen receptor-expressing MCF-7cells, INT J RAD B, 77(9), 2001, pp. 955-962
Citations number
23
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Experimental Biology
Journal title
INTERNATIONAL JOURNAL OF RADIATION BIOLOGY
ISSN journal
0955-3002 → ACNP
Volume
77
Issue
9
Year of publication
2001
Pages
955 - 962
Database
ISI
SICI code
0955-3002(200109)77:9<955:COIDIN>2.0.ZU;2-E
Abstract
Purpose: To compare the cytotoxicity of I-125-oestrogen (E-17 alpha[I-125]i odovinyl-11 beta methoxyoestradiol or (125)IVME2) decay accumulation in hum an breast adenocarcinoma cells that do not express oestrogen receptor (ER) (MDA-231 cells) with human breast adenocarcinoma cells that do express ER ( MCF-7 cells). Materials and methods: MDA-231 cells were labelled with (125)IVME2 or [I-12 5]iododeoxyuridine ((125)IdU), frozen for decay accumulation, thawed and th en plated for colony formation. gamma -irradiation survival was also determ ined. A whole-cell H-3-oestrogen-binding assay and a specific-binding assay were used to detect ER. Results: No MDA-231 cell killing by accumulated (125)IVME2 decays (up to 44 0 dpc) was observed but ER-positive MCF-7 cells were killed by (125)IVME2 ( D-o = 28 dpc). MDA-231 cells were not significantly more radioresistant to gamma -rays (D-o =1.7 Gy for MDA-231 cells 1 Gy for MCF-7 cells) or to (125 )IdU decays (D-o = 44 dpc for MDA-231 cells: 30 dpc For MCF-7 cells). No ER were detected in MDA-231 cells. Conclusions: ER-negative cells, MDA-231, are not killed by (125)IVME2 decay accumulation. It is speculated that without ER (required to translocate th e (125)IVME2 to its nuclear target), formation of the (125)IVME2 ER DNA oes trogen response element (ERE) complex and subsequent specific irradiation o f the DNA at the ERE cannot occur. These results support the hypothesis tha t the nuclear genome is a critical target for radiation-induced cell death.