1999 Fiscal Year Final Research Report Summary
Study for tumor cell-stromal cell interaction related with Platelet-derived growth factor produced by ovarian cancer
| Project/Area Number |
10671552
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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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) |
KAKU Tunehisa Kyushu Univ., School of Health Science, Associate Professor, 医療技術短期大学部, 助教授 (60185717)
HIRAKAWA Toshio Kyushu Univ., Faculty of Medicine, Senior Lecturer, 医学部, 講師 (20218770)
KATO Kiyoko Kyushu Univ., Medical Institute of Bioregulation, Senior Lecturer, 生体防衛医学研究所, 講師 (10253527)
KAMURA Toshiharu Kyushu Univ., Faculty of Medicine, Associate Professor, 医学部, 助教授 (30152870)
WAKE Norio Kyushu Univ., Medical Institute of Bioregulation, Professor, 生体防衛医学研究所, 教授 (50158606)
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| Project Period (FY) |
1998 – 1999
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| Keywords | Ovarian cancer / calponin / PDGF / Cell-cell interaction / Cancer invasion |
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| Research Abstract |
Platelet-derived growth factor (PDGF), sis-oncogene product, was rarely detected in the fluid of benign ovarian tumors. On the other hand the fluid of borderline malignant ovarian tumors often contained low levels of PDGF and the fluid of most ovarian cancers contained PDGF at much higher levels. A Northern blot analysis revealed that the expression of calponin, one of actin-binding cytoskeletal proteins, in fibroblasts or peritoneal methothelial cells was inhibited by the PDGF-containing conditioned medium (CM) of human ovarian cancer cell lines. We confirmed that human recombinant PDGF also decreased the calponin expression in them in a dose-dependent fashion. Our collaborators, Dr. Shu'nichiro Taniguchi et. al. (Faculty of Medicine, Shinshu University), reported that the calponin gene-knockout mouse showed an enhanced peritoneal dissemination of ovarian cancer, which suggested that the decreased expression of calponin in the host peritoneal methothelial cells was related with the increased invasiveness of ovarian cancer cells.
Therefore, it is possible that an ovarian cancer itself induces an advantage for their invasion and metastasis through tumor cell-stromal cell interaction which producing impairment of host stromal defense mechanism. This hypothesis might be helpful to develop a new treatment strategy against the peritoneal dissemination of human ovarian cancer.
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