2007 Fiscal Year Final Research Report Summary
Identification and clinical application of novel antiapoptotic factor produced from ovarian cancer cells
| Project/Area Number |
18591843
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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 | Wakayama Medical University |
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Principal Investigator |
TANAKA Tetsuji Wakayama Medical University, 医学部, Associated Professor (80275255)
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| Co-Investigator(Kenkyū-buntansha) |
KOKAWA Katsuji Wakayama Medical University, 医学部, Assistant Professor (80254548)
UMESAKI Naohiko Wakayama Medical University, 医学部, Professor (20106339)
UTSUNOMIYA Hirotoshi Wakayama Medical University, 医学部, Assistant Professor (60264876)
YAGI Shigetaka Wakayama Medical University, 医学部, Assistant (60372869)
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| Project Period (FY) |
2006 – 2007
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| Keywords | apoptosis / ovarian cancer / drug resistance |
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| Research Abstract |
The animal center of our university had been contaminated with mouse hepatitis virus from 2006 to 2007. All the experimental animals including our mice were killed at first, and then the center was disinfected. However, 6 months after the disinfection, virus was found out again in the animal center. We changed experimental plans to try more in vitro experiments. In the end of 2007, animal experiments were restarted and we are now performing mouse hybridoma experiments. In 2007, the first head investigator was retired. Therefore, unexpectedly the first experimental plans could not performed completely and now we have been continuing the original plans.
(1) Biochemical characterization of M-cell derived antiapoptotic substances (MAAS): We partially purified MAAS from the culture supernatants and immunized Bal b/c mice to mace specific antibody-producing hybridoma. However, all the immunized mice were killed because of the contamination accident in the animal center. Since reopening of the animal center, animal experiments have been restarted. Establishment of the monoclonal antibody will make possible to isolate pure MAAS molecules and clone their cDNA.
(2) Biological characterization of anti-apoptotic phenomena by MAAS: (1) We have been investigating molecular mechanisms of anticancer drug-induced ovarian failure in the other experiments. By chance, those experiments had found possible antiapoptotic mechanisms similar to MAAS-induced antiapoptosis. (2) We have established several CDDP-resistant cell lines from M cells. Two CDDP-resistant cell lines produced much higher MAAS activity than that the parent cells. These data indicate that increased MAAS activity can be a possible mechanism of an acquired CDDP resistance.
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