Grenman S E, Worsham M J, Van Dyke D L, England B, McClatchey K D, Babu V R, Roberts J A, Mäenpää J, Carey T E
Department of Otolaryngology/Head and Neck Surgery, University of Michigan, Ann Arbor 48109-0506.
Gynecol Oncol. 1990 May;37(2):188-99. doi: 10.1016/0090-8258(90)90332-f.
UM-EC-2 was established from a patient with poorly differentiated stage IB endometrial carcinoma. This cell line produces tumors in nude mice that have the same histological features as the patient's tumor. UM-EC-2 cells express b2-microglobulin, the epidermal growth factor receptor (EGF), and the H blood group antigen. This membrane antigen phenotype is consistent with cells of human endometrial origin. The karyotype of UM-EC-2 is fairly complex, with rearrangements affecting all chromosomes except 3, 10, 14, 19, and 20. There were two populations of cells, a hyperdiploid population with a modal number of 53-55 and a hypertetraploid population with a modal number of 109. A postulated sequence of events before and after tetraploidization is suggested based on the number of copies of individual chromosomes and rearrangements. Comparison of the UM-EC-2 karyotype to that of UM-EC-1 (a previously described line from a different patient with endometrial carcinoma) revealed that the two lines share eight very similar chromosome changes, which include loss of most of chromosome 4, breakpoints affecting proximal bands on 8p, loss of most of 9q, a breakpoint at 12q22, loss of 13q, breakpoints in proximal bands on 18q, and a breakpoint at 22p11. These changes may represent nonrandom chromosome abnormalities in poorly differentiated endometrial cancer. Estrogen (ER) and progesterone (PgR) receptors were not detected in either the primary tumor or the cell line. Nevertheless, UM-EC-2 cells were very sensitive to growth inhibition by tamoxifen (TAM) in vitro. One micromolar TAM caused 50% inhibition of cell growth, 2.5 microM caused cytostasis, and 5 microM TAM was cytotoxic, killing all cells after 5-7 days of exposure to the drug. Paradoxically, 100 nM estradiol (E2) caused a moderate increase in the growth of the cells but it did not prevent or reverse growth inhibitory effects of TAM. These findings support the concept that in some tumors TAM causes growth inhibition by an ER-independent mechanism. UM-EC-2 cells were also sensitive to growth regulation by EGF. Thus, these cells provide a new in vitro model of human endometrial cancer in which the roles of both TAM and EGF as growth regulatory substances can be investigated.
UM-EC-2源自一名低分化IB期子宫内膜癌患者。该细胞系在裸鼠体内产生的肿瘤具有与患者肿瘤相同的组织学特征。UM-EC-2细胞表达β2-微球蛋白、表皮生长因子受体（EGF）和H血型抗原。这种膜抗原表型与人类子宫内膜来源的细胞一致。UM-EC-2的核型相当复杂，除3、10、14、19和20号染色体外，所有染色体均发生重排。存在两个细胞群体，一个超二倍体群体，众数为53 - 55，一个超四倍体群体，众数为109。根据单个染色体的拷贝数和重排情况，推测了四倍体化前后的一系列事件。将UM-EC-2的核型与UM-EC-1（先前描述的来自另一名子宫内膜癌患者的细胞系）的核型进行比较，发现这两个细胞系共有八个非常相似的染色体变化，包括4号染色体大部分缺失、8p近端带的断点、9q大部分缺失、12q22处的断点、13q缺失、18q近端带的断点以及22p11处的断点。这些变化可能代表低分化子宫内膜癌中的非随机染色体异常。在原发性肿瘤或细胞系中均未检测到雌激素（ER）和孕激素（PgR）受体。然而，UM-EC-2细胞在体外对他莫昔芬（TAM）的生长抑制非常敏感。1微摩尔TAM可导致50%的细胞生长抑制，2.5微摩尔导致细胞生长停滞，5微摩尔TAM具有细胞毒性，在接触药物5 - 7天后杀死所有细胞。矛盾的是，100纳摩尔雌二醇（E2）可使细胞生长适度增加，但它并未阻止或逆转TAM的生长抑制作用。这些发现支持了在某些肿瘤中TAM通过非雌激素受体依赖机制导致生长抑制的概念。UM-EC-2细胞对EGF的生长调节也很敏感。因此，这些细胞提供了一种新的人类子宫内膜癌体外模型，可用于研究TAM和EGF作为生长调节物质的作用。
