1999 Fiscal Year Final Research Report Summary
Study on Apoptotic cell death and mechanism of metastasis of adenoid cystic carcinoma derived cell line.
| Project/Area Number |
10671876
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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 |
Surgical dentistry
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| Research Institution | Tottori University |
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Principal Investigator |
RYOKE Kazuo Tottori University, Medicine, Professor., 医学部, 教授 (20093635)
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| Co-Investigator(Kenkyū-buntansha) |
KATAOKA Satoshi Tottori University, Medicine, Assistant., 医学部, 助手 (20283989)
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| Project Period (FY) |
1998 – 1999
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| Keywords | ACC-3 / Apoptosis / 5-Fluorouracil / Nedaplation / Carboplation / p53 / VEGF |
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| Research Abstract |
We investigated on cell death in cultured human adenoid cystic carcinoma cell line (ACC-3) induced by anti-cancer drugs of 5-Fluorouracil (5-Fu), Nedaplatin (Ned) and Carboplatin (CBDCA), added to apoptosis of such cell line.
We also investigated on squamous cell carcinoma such as HSC-2, HSC-3, HSC-4 and Ca9-22 in addition to ACC-3.
We investigated growth-inhibitory effect of 5-Fu was the most prominent in Ca 9-22, followed by ACC-3 and HSC-4, but no any effects were found in HSC-2 and HSC-3. As for Ned, the growth-inhibitory effects were obtained in all cell lines tested, the most prominent in HSC-3, followed by HSC-4, Ca9-22, HSC-2 and ACC-3(55%). The growth-inhibitory effect of CBDCA was the most prominent in HSC-2, followed by HSC-4, HSC-3 and Ca9-22(60%).
By TUNEL method apoptosis of tumor cell lines were estimated with apoptotic index (AI). AI of HSC-3, HSC-2, HSC-4 and ACC-3 with 5-Fu after 24 hours were 12%, 10%, 8% and 2% respectively.
As for Ned the AI of HSC-3, HSC-4 and ACC-3 were 3%, 9% and 6%, respectively. As for CBDCA AI of ACC-3 was 3%.
Induction mechanism of apoptosis was intended to be obvious with confirming effect individually in each of 5-Fu, Ned and CBDCA was ascertained, so relation to distant metestasis was investigated with examining of VEGF in addition to p53. As a result, relationship of p53 and VEGF was distinct.
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