Interleukin-1 as an Autocrine Stimulator in the Growth of Human Ovarian Cancer Cells
Hiroshima Journal of Medical Sciences 46 巻 1 号
51-59 頁
1997-03 発行
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種類 :
全文
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タイトル ( eng ) |
Interleukin-1 as an Autocrine Stimulator in the Growth of Human Ovarian Cancer Cells
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作成者 |
Kawakami Yosuke
Nagai Nobutaka
Ota Sanae
Ohama Koso
Yamashita Uki
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収録物名 |
Hiroshima Journal of Medical Sciences
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巻 | 46 |
号 | 1 |
開始ページ | 51 |
終了ページ | 59 |
収録物識別子 |
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
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抄録 |
The role of interleukin-1 (IL-1), a multifunctional cytokine which mediates important immune responses, was investigated in the growth of ovarian cancer cell lines in vitro. The messenger RNA for IL-1α and IL-1β was expressed in six and four ovarian cancer cell lines, respectively out of eight. Measurement of IL-1 in the eight cell lines by enzyme-linked immunosorbent assay revealed that two lines, MCAS and TYK-nu, secreted a high amount of IL-1α, but that none secreted IL-1βafter 72 hours of incubation. The growth of these cells was significantly stimulated by the addition of recombinant IL-1α(rIL-1α) in a concentration-dependent manner in a 96 hour culture. The maximum response was obtained with 10 ng/ml of IL-1αby counting the viable cell number using trypan blue. [3H]-thymidine incorporation by these cells was also stimulated by a 72 hour incubation with rIL-1α. The spontaneous growth of these cells was inhibited by the addition of anti-IL-1αantibody, anti-IL-1 receptor antibody or IL-1 receptor antagonist. These cells expressed two classes of IL-1-binding receptors on their surface as detected by [125I]-labeled rIL-1α. These results indicate that IL-1αis an autocrine growth stimulator for some ovarian cancer cells and suggest that IL-1αplays an important role in the progression of this disease.
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著者キーワード |
IL-1
Autocrine stimulation
Ovarian cancer cells
EGF receptor
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NDC分類 |
医学 [ 490 ]
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言語 |
英語
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資源タイプ | 紀要論文 |
出版者 |
Hiroshima University Medical Press
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発行日 | 1997-03 |
出版タイプ | Version of Record(出版社版。早期公開を含む) |
アクセス権 | オープンアクセス |
収録物識別子 |
[ISSN] 0018-2052
[NCID] AA00664312
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