趋化因子（C-C基序）配体-2（CCL2）在卵巢腺癌中的表达降低。

Arnold J M, Huggard P R, Cummings M, Ramm G A, Chenevix-Trench G

The Queensland Institute of Medical Research, c/o RBH Post Office, Herston, Brisbane, QLD 4029, Australia.

Br J Cancer. 2005 Jun 6;92(11):2024-31. doi: 10.1038/sj.bjc.6602596.

Chemokine (C-C motif) ligand-2 (CCL2) is a chemoattractant and activator of macrophages and is a key determinant of the macrophage infiltrate into tumours. We demonstrate here that CCL2 is expressed in normal human ovarian surface epithelium (HOSE) cells and is silenced in most ovarian cancer cell lines, and silenced or downregulated in the majority of primary ovarian adenocarcinomas. Analysis of the CCL2 locus at 17q11.2-q12 showed loss of heterozygosity (LOH) in 70% of primary tumours, and this was significantly more common in tumours of advanced stage or grade. However, we did not detect any mutations in the CCL2 coding sequence in 94 primary ovarian adenocarcinomas. These data support the hypothesis that CCL2 may play a role in the pathobiology of ovarian cancers, but additional studies will be required to evaluate this possibility.

趋化因子（C-C基序）配体2（CCL2）是巨噬细胞的趋化剂和激活剂，是巨噬细胞浸润肿瘤的关键决定因素。我们在此证明，CCL2在正常人类卵巢表面上皮（HOSE）细胞中表达，而在大多数卵巢癌细胞系中沉默，并在大多数原发性卵巢腺癌中沉默或下调。对17q11.2-q12处CCL2基因座的分析显示，70%的原发性肿瘤存在杂合性缺失（LOH），这在晚期或高级别肿瘤中更为常见。然而，我们在94例原发性卵巢腺癌的CCL2编码序列中未检测到任何突变。这些数据支持CCL2可能在卵巢癌病理生物学中起作用的假设，但需要进一步研究来评估这种可能性。