1993 Fiscal Year Final Research Report Summary
Inhibition of Estrogen Responsive Cell Growth in Human Breast Cancer by Antisense c-myc phosphorothioate Oligonucleotide.
| Project/Area Number |
04670740
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
General surgery
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
UEO Hiroaki Medical Institute of Bioregulation, Kyushu University, Associate Professor., 生体防御医学研究所, 助教授 (70150430)
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| Co-Investigator(Kenkyū-buntansha) |
MURAKAMI Akira Faculty of Textile Science, Kyoto Institute of Technology, Professor, 繊維学部, 教授 (60210001)
SHIBUTA Kenji Medical Institute of Bioregulation, Kyushu University, Lecture, 生体防御医学研究所, 助手 (70253531)
NAKASHIMA Hideaki Medical Institute of Bioregulation, Kyushu University, Lecture, 生体防御医学研究所, 助手 (20253528)
INOUE Hiroshi Medical Institute of Bioregulation, Kyushu University, Lecture, 生体防御医学研究所, 助手 (90203249)
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| Project Period (FY) |
1992 – 1993
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| Keywords | Antisense oligonucleotide / c-myc / gene therapy / estrogen responsiveness |
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| Research Abstract |
To investigate the role of c-myc in the growth of estrogen(E2)-responsive human breast cancer cells, we examined the in vitro effects of a synthetic antisense c-myc phosphorotioate oligonucleotide both on E2-stimulated cell growth of a human breast cancer cell line, MCF-7, and E2-induced growth inhibition of an ES-1 cell line, a mutant of MCF-7. Flowcytometric analysis showed that the FITC-labeled antisense c--myc(10mM) was taken up by more than 90% of the cells within 24 hours incubation. Antisense c-myc significantly suppressed c-myc protein expression and inhibited the E2-stimulating cell growth of MCF-7 cells. The cell growth of ES-1 cells, maintained with E2-deprived medium, was also inhibited by antisense c-myc and E2-induced growth inhibition was not blocked by the antisense c-myc. These results indicate that antisense c-myc phosphorothioate oligonucleotide can suppress c-myc gene expression and thus inhibit both E2-dependent and E2-independent cell growth of human breast cancer.
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