1999 Fiscal Year Final Research Report Summary
Laryngeal Cancer Cell Death; Mutotion of Androgen Receptor Gene
| Project/Area Number |
09671767
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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 |
Otorhinolaryngology
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| Research Institution | St. Marianna University School of Medicine |
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Principal Investigator |
TAMOTUSU Urushibata St.Marianna Unive. Schoold of Med, Dept.of ORL, Assistant Professor, 医学部, 講師 (70130987)
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| Project Period (FY) |
1997 – 1999
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| Keywords | Laryngeal / Laryngeal Cancer / Cell death / Androgen / Receptor / CAG tandem Repeat / Mutation |
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| Research Abstract |
Based on human phonetic differentiation of both sexed and the etiologic finding of laryngeal cancer, androgen would be regarded as significant factor on the development of laryngeal tissue and serious etiologic factor of male-predominant laryngeal cancer. In this study, a laryngeal carcinoma cell line (Hip-2) was examined on the expression of AR protein and mRNA, and responsiveness to androgen, related with the cell proliferation. Immunohistochemical study and electrophoresis of RT-PCR product showed Hep-2 cell expressing AR protein and mRNA, using primers which produce nucleotide sequence of AR between 70 through 367 from the start codon, respectively. The band of gel, however, showed Hep-2 expressing a bit short sized AR mRNA, compared with control. Nucleotide sequential analysis showed that the AR is existence of gene mutation, deleting 9 CAG tandem repeats in the coding modulator region. Above 1 μM, testosterone propionate (TP) induced cell death up to 99%, 3 days after the administration. Immunohistochemical study suggested that Hep-2 cells incorporated TP into their nuclei only through the specific AR and came to cell death, accompanied by enhanced expression of P53, bcl-2 and bax proteins. These data implied that the expression of mutated AR deleting 9 glutamines in the modulator region, combined with androgenic steroids, could trigger the cascade of cell death in Hep-2 cell line.
Supported in part by GASRc9671767.
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