Cancer cachexia syndrome developed in nude mice bearing melanoma cells producing leukemia-inhibitory factor.
Cancer cachexia syndrome developed in nude mice bearing melanoma cells producing leukemia-inhibitory factor.
复制标题
携带产生白血病抑制因子的黑色素瘤细胞的裸鼠出现癌症恶病质综合征。
作者：
M. Mori;K. Yamaguchi;S. Honda;K. Nagasaki;M. Ueda;O. Abe;K. Abe
黑色素瘤衍生脂蛋白脂酶抑制剂（MLPLI）是从人黑色素瘤细胞系SEKI的条件培养基中纯化的因子，其在荷瘤裸鼠中诱导严重恶病质。氨基酸序列分析表明，氨基端部分是相同的白血病抑制因子（LIF）。为了确定MLPLI是否实际上是LIF，在SEKI黑素瘤细胞系中检查LIF mRNA的表达。北方印迹分析显示，该细胞系显示出分子大小为3.8个丝氨酸的强杂交条带，表明MLPLI与LIF相同。癌性恶病质综合征的发展和LIF mRNA的表达之间的关系进行了检查，在四个黑色素瘤异种移植，SEKI，G361，A375和MEWO，在裸鼠。SEKI和G361荷瘤裸鼠出现癌性恶病质综合征，移植后第25天体重分别下降至对照组的73.6%和73.8%。然而，A375和MEWO荷瘤裸鼠没有出现这种综合征。北方印迹分析显示，G361和SEKI表达大量LIF mRNA，而A375和MEWO不表达，提示LIF mRNA的表达与综合征的发生密切相关。这些数据支持MLPLI或LIF在荷黑色素瘤裸鼠中观察到的癌症恶病质综合征的发展中起重要作用的概念。
Melanoma-derived lipoprotein lipase inhibitor (MLPLI) is a factor purified from the conditioned medium of a human melanoma cell line, SEKI, which induced severe cachexia in tumor-bearing nude mice. Amino acid sequencing revealed that the amino-terminal portion was identical to that of leukemia-inhibitory factor (LIF). To determine whether MLPLI is actually LIF, the expression of LIF mRNA was examined in the SEKI melanoma cell line. Northern blot analyses revealed that the cell line displayed an intense hybridizable band with a molecular size of 3.8 kilobases, suggesting that MLPLI is identical to LIF. The relationship between the development of the cancer cachexia syndrome and the expression of LIF mRNA was examined in four melanoma xenografts, SEKI, G361, A375 and MEWO, in nude mice. SEKI- and G361-bearing nude mice developed cancer cachexia syndrome, and their body weights decreased by the 25th day after the transplantation to 73.6% and 73.8% of the control, respectively. A375- and MEWO-bearing nude mice, however, did not develop the syndrome. Northern blot analyses revealed that G361 as well as SEKI expressed a large amount of LIF mRNA, but A375 and MEWO did not, suggesting a close relationship between the expression of LIF mRNA and the development of the syndrome. These data support the concept that MLPLI, or LIF, plays an important role in the development of the cancer cachexia syndrome observed in melanoma-bearing nude mice.