| Project/Area Number |
06671665
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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 |
Obstetrics and gynecology
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| Research Institution | Kyushu University |
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Principal Investigator |
KOBAYASHI Hiroaki Kyushu Univ., Faculty of Medicine, Lecturer, 医学部, 助手 (70260700)
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| Co-Investigator(Kenkyū-buntansha) |
OKADOME Masao Kyushu Univ., Faculty of Medicine, Lecturer, 医学部, 助手 (30260699)
SAITO Toshiaki Kyushu Univ., Faculty of Medicine, Senior Lecturer, 医学部, 講師 (80162212)
KAMURA Toshiharu Kyushu Univ., Faculty of Medicine, Associate Professor, 医学部, 助教授 (30152870)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1994: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Ovarian cancer / Interleukin-6 / Antisense Oligonucleotide / Autocrine Growth Factor |
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| Research Abstract |
Interleukin-6 (IL-6) is a multifunctional cytokine which has been reoently reported to be produced by human ovarian cancer. To evaluate the effects of IL-6 on the growth of ovarian cancer, we used 11 human ovarian cancer cell lines and got the results as follows :
1.All of 10 epithelial-originated ovarian cancer cell lines produced bioactive IL-6. On the other hand, one ovarian cancer cell line of non-epithelial-origin did not release detectable IL-6 into its culturemedium.
2.Antisense oligonucleotide for IL-6 specifically inhibited both cell growth and the IL-6-production of all IL-6-producing ovarian cancer cell lines. The growth inhibitory effect of the antisense oligonucleotide could be diminished not the co-administration of exogenous IL-6 but by the co-administration of IL-6-sense oligonucleotide.
3.The specific growth inhibitory activity of IL-6-antisense oligonucleotide was not be observed in the case of IL-6-non-producing ovarian cancer cell line.
4.The growth potential of all ovarian cancer cell lines was affected by neither recombinant human IL-6 nor its neutralizing antibody.
5.By the analysis for gene expression of IL-6 receptor and gp130 signal transducer, four of ten IL-6-producing ovarian cancer cell lines seemed to possess the ability to mediate the signal of extracellular IL-6. The other six Il-6-producing cell lines and an IL-6-non-producing cell line did not express IL-6 receptor.
These results suggest that endogenous IL-6 produced by ovarian cancer cells may behave as a growth stimulator by an intracellular autocrine mechanism not involving a mechanism through the cell membrane, although further studies are required to verify this hypothesis.
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