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

为探讨口腔鳞状细胞癌患者血清二肽基肽酶IV活性下降的原因，分析了恶性细胞源性细胞因子对人T细胞表面二肽基肽酶IV(CD26/DPP IV)表达的影响。KB细胞产生细胞因子，尤其是25 kDa的成熟β-DPPIV下调T细胞CD26DPPIV的表达，这是导致培养上清液中DPPIV活性降低的原因之一。KBCM诱导的T细胞G1期停滞外，T细胞中p27^-kip&gt；的表达水平保持不变，并可被抗转化生长因子-β-1抗体中和所抑制。由KB细胞产生的成熟的转化生长因子-β1下调T细胞CD2 6/DPPIV的表达，同时通过维持p2 7；；kip&gt；的表达抑制T细胞的生长，导致细胞周期停滞于G1期，支持了恶性细胞衍生的可溶性因子抑制T细胞的细胞增殖、细胞激活和免疫功能的概念，从而导致肿瘤标志物、口腔癌患者血清CD2 6/DPPIV活性的下降。

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.