Kawakami M, Kondo Y, Imai Y, Hashiguchi M, Ogawa H, Hiragun A, Aotsuka S, Shibata S, Oda T, Murase T
Clinical Research Institute, National Medical Center Hospital, Tokyo.
J Biochem. 1991 Jan;109(1):78-82.
Production of a cachexia-inducing factor(s) by the SEKI melanoma cell line, established from a human melanoma, has been well documented. Conditioned medium from cultures of this melanoma cell line contains a factor(s) that inhibits the activity of lipoprotein lipase (LPL) in fully differentiated 3T3-L1 adipocytes. The mode of inhibition of this enzyme by the factor, i.e. its dose-dependency and time course, is very similar to that of LPL-inhibition by a macrophage-derived cachexia-inducing factor, cachectin/tumor necrosis factor (cachectin/TNF). However, the conditioned medium of SEKI melanoma cells does not contain any immuno-reactive substances reactive in enzyme-linked immunosorbent assay (ELISA) with anti-cachectin/TNF antibody, or with anti-interleukin 1 alpha or beta antibodies. This LPL-suppression factor present in the conditioned medium seems to be a peptide because of its heat-lability and apparent molecular weight of more than 25,000. The conditioned media from cultures of four other different cell lines were found to show no significant suppression of LPL activity. These results imply that SEKI melanoma cells produce a cachexia-inducing factor(s) similar to cachectin/TNF but that the molecule involved is different.
从一名人类黑色素瘤患者身上建立的SEKI黑色素瘤细胞系能够产生恶病质诱导因子，这一点已有充分记录。该黑色素瘤细胞系培养物的条件培养基中含有一种因子，可抑制完全分化的3T3-L1脂肪细胞中脂蛋白脂肪酶（LPL）的活性。该因子对这种酶的抑制模式，即其剂量依赖性和时间进程，与巨噬细胞衍生的恶病质诱导因子、恶病质素/肿瘤坏死因子（恶病质素/TNF）对LPL的抑制模式非常相似。然而，SEKI黑色素瘤细胞的条件培养基中不含有任何在酶联免疫吸附测定（ELISA）中与抗恶病质素/TNF抗体、或抗白细胞介素1α或β抗体发生反应的免疫反应性物质。由于其热稳定性和明显超过25,000的分子量，条件培养基中存在的这种LPL抑制因子似乎是一种肽。另外四种不同细胞系培养物的条件培养基未显示出对LPL活性的显著抑制作用。这些结果表明，SEKI黑色素瘤细胞产生了一种与恶病质素/TNF类似的恶病质诱导因子，但所涉及的分子不同。
