2001 Fiscal Year Final Research Report Summary
SERUM DIPEPTIDYLPEPTIDASE(DPP)IV AS A POSSIBLE MARKER ENZYME OF ORAL CANCER
| Project/Area Number |
10470444
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | MATSUMOTO DENTAL UNIVERSITY |
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Principal Investigator |
UEMATSU Takashi MATSUMOTO DENTAL UNIVERSITY, FACULTY OF DENTISTRY, ASSOCIATE PROFESSOR, 歯学部, 助教授 (40203476)
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| Co-Investigator(Kenkyū-buntansha) |
TANAKA Hitoshl MATSUMOTO DENTAL UNIVERSITY, FACULTY OF DENTISTRY, ASSISTANT PROFESSOR, 歯学部, 助手 (50267788)
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| Project Period (FY) |
1998 – 2001
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| Keywords | ジペチジルペプチダーゼ IV / CD26 / 口腔癌 / T細胞 / TGF-β1 / 免疫抑制 / マーカーエンザイム |
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| Research Abstract |
To clarify the cause of the decrease in serum dipeptidyl peptidase (DPP) IV activity in patients with oral squamous cell carcinoma, the influence of malignant cell-derived cytokines to the cell surface DPPIV (CD26 / DPP IV) expression in human T cells was analyzed.
Decrease in CD26/DPPIV expression of T cell extract and culture supernatant was found in the 8-30 kDa fraction of KBCM. KB cells produced cytokines, especially 25 kDa of mature TGF-β1 downregulated CD26/ DPPIV expression in T cells, which was responsible for decreased DPPIV activity in the cultured supernatant. The level of p27^<kip> expression in T cells was maintained in addition to T cell G1 arrest in the cultivation with KBCM and was abolished by neutralizing anti-TGF-β1 antibody. :
Mature TGF-β1 produced by KB cells down-regulates the CD26/DPPIV expression in T cells concomitant with the suppression of T cell growth by maintaining p27^<kip> expression, which leads to a cell cycle arrest in G1, supporting the concept that malignant cell-derived soluble factors inhibit cell proliferation, cell activation and immune function in T cells resulting in a decrease in the tumor marker, serum CD26/DPPIV activity of oral cancer patients.
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Research Products
(4 results)
