Kimmel Cancer Center, Department of Cancer Biology and Stem Cell Biology and Regenerative Medicine, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Cancer Res. 2012 Aug 1;72(15):3839-50. doi: 10.1158/0008-5472.CAN-11-3917. Epub 2012 May 25.
The roles of the chemokine CCL5 and its receptor CCR5 in breast cancer progression remain unclear. Here, we conducted microarray analysis on 2,254 human breast cancer specimens and found increased expression of CCL5 and its receptor CCR5, but not CCR3, in the basal and HER-2 genetic subtypes. The subpopulation of human breast cancer cell lines found to express CCR5 displayed a functional response to CCL5. In addition, oncogene transformation induced CCR5 expression, and the subpopulation of cells that expressed functional CCR5 also displayed increased invasiveness. The CCR5 antagonists maraviroc or vicriviroc, developed to block CCR5 HIV coreceptor function, reduced in vitro invasion of basal breast cancer cells without affecting cell proliferation or viability, and maraviroc decreased pulmonary metastasis in a preclinical mouse model of breast cancer. Taken together, our findings provide evidence for the key role of CCL5/CCR5 in the invasiveness of basal breast cancer cells and suggest that CCR5 antagonists may be used as an adjuvant therapy to reduce the risk of metastasis in patients with the basal breast cancer subtype.
趋化因子 CCL5 及其受体 CCR5 在乳腺癌进展中的作用尚不清楚。在这里,我们对 2254 个人类乳腺癌标本进行了微阵列分析,发现基底和 HER-2 遗传亚型中 CCL5 和其受体 CCR5 的表达增加,但 CCR3 没有增加。表达 CCR5 的人乳腺癌细胞系亚群表现出对 CCL5 的功能反应。此外,致癌基因转化诱导 CCR5 的表达,并且表达功能性 CCR5 的细胞亚群也表现出侵袭性增加。开发用于阻断 CCR5 HIV 辅助受体功能的 CCR5 拮抗剂 maraviroc 或 vicriviroc,降低了体外基底乳腺癌细胞的侵袭性,而不影响细胞增殖或活力,并且 maraviroc 降低了乳腺癌临床前小鼠模型中的肺转移。总之,我们的研究结果为 CCL5/CCR5 在基底乳腺癌细胞侵袭性中的关键作用提供了证据,并表明 CCR5 拮抗剂可用作辅助治疗,以降低基底乳腺癌亚型患者的转移风险。