SERUM DIPEPTIDYLPEPTIDASE(DPP)IV AS A POSSIBLE MARKER ENZYME OF ORAL CANCER

为阐明口腔鳞状细胞癌患者血清二肽基肽酶（DPP） IV活性降低的原因，分析了恶性细胞源性细胞因子对人T细胞表面DPPIV （CD26 / DPPIV）表达的影响。8 ~ 30 kDa部位的T细胞提取物和培养上清CD26/DPPIV表达均降低。KB细胞产生细胞因子，特别是25 kDa的成熟TGF-β1下调T细胞中CD26/ DPPIV的表达，这是培养上清中DPPIV活性降低的原因。在KBCM培养中，除了T细胞G1阻滞外，T细胞中p27^<kip>的表达水平保持不变，并通过中和抗tgf -β1抗体而被消除。：成熟的KB细胞产生的TGF-β1通过维持p27^<kip>的表达，下调T细胞中CD26/DPPIV的表达，同时抑制T细胞生长，导致细胞周期阻滞在G1期，支持恶性细胞源性可溶性因子抑制T细胞增殖、细胞活化和免疫功能，导致口腔癌患者肿瘤标志物血清CD26/DPPIV活性降低的观点。

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.