Weber Günther, Chamorro Clara Ibel, Granath Fredrik, Liljegren Annelie, Zreika Sami, Saidak Zuzana, Sandstedt Bengt, Rotstein Samuel, Mentaverri Romuald, Sánchez Fabio, Pivarcsi Andor, Ståhle Mona
GICC, CNRS UMR 6239, Université François Rabelais, Avenue Monge, Tours, France.
Breast Cancer Res. 2009;11(1):R6. doi: 10.1186/bcr2221. Epub 2009 Jan 30.
Human cathelicidin antimicrobial protein, hCAP18, and its C-terminal peptide LL-37 is a multifunctional protein. In addition to being important in antimicrobial defense, it induces chemotaxis, stimulates angiogenesis and promotes tissue repair. We previously showed that human breast cancer cells express high amounts of hCAP18, and hypothesised that hCAP18/LL-37 may be involved in tumour progression.
hCAP18 mRNA was quantified in 109 primary breast cancers and compared with clinical findings and ERBB2 mRNA expression. Effects of exogenous LL-37 and transgenic overexpression of hCAP18 on ErbB2 signalling were investigated by immunoblotting using extracts from breast cancer cell lines ZR75-1 and derivatives of MCF7. We further analysed the impact of hCAP18/LL-37 on the morphology of breast cancer cells grown in soft agar, on cell migration and on tumour development in severe combined immunodeficiency (SCID) mice.
The expression of hCAP18 correlated closely with that of ERBB2 and with the presence of lymph node metastases in oestrogen receptor-positive tumours. hCAP18/LL-37 amplified Heregulin-induced mitogen-activated protein kinase (MAPK) signalling through ErbB2, identifying a functional association between hCAP18/LL-37 and ErbB2 in breast cancer. Treatment with LL-37 peptide significantly stimulated the migration of breast cancer cells and their colonies acquired a dispersed morphology indicative of increased metastatic potential. A truncated version of LL-37 competitively inhibited LL-37 induced MAPK phosphorylation and significantly reduced the number of altered cancer cell colonies induced by LL-37 as well as suppressed their migration. Transgenic overexpression of hCAP18 in a low malignant breast cancer cell line promoted the development of metastases in SCID mice, and analysis of hCAP18 transgenic tumours showed enhanced activation of MAPK signalling.
Our results provide evidence that hCAP18/LL-37 contributes to breast cancer metastasis.
人阳离子抗菌蛋白hCAP18及其C端肽LL-37是一种多功能蛋白。除了在抗菌防御中起重要作用外,它还能诱导趋化作用、刺激血管生成并促进组织修复。我们之前发现人乳腺癌细胞大量表达hCAP18,并推测hCAP18/LL-37可能参与肿瘤进展。
对109例原发性乳腺癌中的hCAP18 mRNA进行定量,并与临床结果及ERBB2 mRNA表达进行比较。使用乳腺癌细胞系ZR75-1和MCF7衍生物的提取物,通过免疫印迹法研究外源性LL-37和hCAP18转基因过表达对ErbB2信号传导的影响。我们进一步分析了hCAP18/LL-37对软琼脂中生长的乳腺癌细胞形态、细胞迁移以及严重联合免疫缺陷(SCID)小鼠肿瘤发展的影响。
hCAP18的表达与ERBB2的表达以及雌激素受体阳性肿瘤中淋巴结转移的存在密切相关。hCAP18/LL-37通过ErbB2放大了Heregulin诱导的丝裂原活化蛋白激酶(MAPK)信号传导,确定了hCAP18/LL-37与乳腺癌中ErbB2之间的功能关联。用LL-37肽处理显著刺激了乳腺癌细胞的迁移,并且它们的集落获得了分散的形态,表明转移潜能增加。LL-37的截短版本竞争性抑制LL-37诱导的MAPK磷酸化,并显著减少LL-37诱导的改变的癌细胞集落数量以及抑制它们迁移。hCAP18在低恶性乳腺癌细胞系中的转基因过表达促进了SCID小鼠中转移灶的形成,并且对hCAP18转基因肿瘤的分析显示MAPK信号传导的激活增强。
我们的结果提供了证据表明hCAP18/LL-37促成乳腺癌转移。