Mori M, Yamaguchi K, Abe K
Growth Factor Division, National Cancer Center Research Institute, Tokyo, Japan.
Biochem Biophys Res Commun. 1989 May 15;160(3):1085-92. doi: 10.1016/s0006-291x(89)80114-7.
A human melanoma cell line, SEKI, induces severe cachexia in tumor-bearing nude mice. A factor with the ability to inhibit lipoprotein lipase (LPL) was isolated from the conditioned medium of this cell line. This factor was 40-K-dalton protein, and designated temporarily as melanoma-derived LPL inhibitor (MLPLI). Amino acid sequencing revealed that the amino-terminal portion consists of SPLPITPV-AT--IR-P. Unexpectedly, the sequence, as far as determined, was identical to those of leukemia inhibitory factor (LIF), suggesting that MLPLI is a protein closely related to LIF. The findings that MLPLI inhibits LPL activity and that MLPLI is produced by human cancer cells inducing cancer cachexia also suggest that this protein is a candidate for the factor responsible for cancer cachexia.
一种人黑色素瘤细胞系SEKI可在荷瘤裸鼠中诱导严重的恶病质。从该细胞系的条件培养基中分离出一种具有抑制脂蛋白脂肪酶（LPL）能力的因子。该因子是一种40千道尔顿的蛋白质，暂时命名为黑色素瘤衍生的LPL抑制剂（MLPLI）。氨基酸测序显示，其氨基末端部分由SPLPITPV-AT--IR-P组成。出乎意料的是，就已确定的序列而言，它与白血病抑制因子（LIF）的序列相同，这表明MLPLI是一种与LIF密切相关的蛋白质。MLPLI抑制LPL活性以及MLPLI由诱导癌症恶病质的人类癌细胞产生的这些发现也表明，这种蛋白质是导致癌症恶病质的因子的候选者。
