Bouchard Gina, Therriault Hélène, Geha Sameh, Bujold Rachel, Saucier Caroline, Paquette Benoit
Centre for Research in Radiotherapy, Department of Nuclear Medicine and Radiobiology, Faculty of Medicine and Health Sciences, Sherbrooke, Québec, Canada.
Department of Pathology, Centre Hospitalier Universitaire de Sherbrooke, Sherbrooke, Québec, Canada.
Br J Cancer. 2017 Feb 14;116(4):479-488. doi: 10.1038/bjc.2016.448. Epub 2017 Jan 19.
The prognosis of triple-negative breast cancer (TNBC) is still difficult to establish. Some TNBC benefit from radiotherapy (RT) and are cured, while in other patients metastases appear during the first 3 years after treatment. In this study, an animal model of TNBC was used to determine whether the expression of the cell membrane protease MT1-MMP in cancer cells was associated with radiation-stimulated development of lung metastases.
Using invasion chambers, irradiated fibroblasts were used as chemoattractants to assess the invasiveness of TNBC D2A1 cell lines showing downregulated expression of MT1-MMP, which were compared with D2A1-wt (wild-type) and D2A1 shMT1-mock (empty vector) cell lines. In a mouse model, a mammary gland was irradiated followed by the implantation of the downregulated MT1-MMP D2A1, D2A1-wt or D2A1 shMT1-mock cell lines. Migration of D2A1 cells in the mammary gland, number of circulating tumour cells and development of lung metastases were assessed.
The reduction of MT1-MMP expression decreased the invasiveness of D2A1 cells and blocked the radiation enhancement of cancer cell invasion. In BALB/c mice, irradiation of the mammary gland has stimulated the invasion of cancer cells, which was associated with a higher number of circulating tumour cells and of lung metastases. These adverse effects of radiation were prevented by downregulating the MT1-MMP.
This study shows that the MT1-MMP is necessary for the radiation enhancement of lung metastasis development, and that its expression level and/or localisation could be evaluated as a biomarker for predicting the early recurrence observed in some TNBC patients.
三阴性乳腺癌(TNBC)的预后仍然难以确定。一些TNBC患者受益于放疗(RT)并得以治愈,而其他患者在治疗后的前3年内会出现转移。在本研究中,使用TNBC动物模型来确定癌细胞中细胞膜蛋白酶MT1-MMP的表达是否与辐射刺激的肺转移发展相关。
使用侵袭小室,将经辐射的成纤维细胞用作趋化因子,以评估MT1-MMP表达下调的TNBC D2A1细胞系的侵袭性,并将其与D2A1-wt(野生型)和D2A1 shMT1-mock(空载体)细胞系进行比较。在小鼠模型中,对乳腺进行辐射,随后植入MT1-MMP表达下调的D2A1、D2A1-wt或D2A1 shMT1-mock细胞系。评估D2A1细胞在乳腺中的迁移、循环肿瘤细胞数量和肺转移的发展情况。
MT1-MMP表达的降低降低了D2A1细胞的侵袭性,并阻断了辐射对癌细胞侵袭的增强作用。在BALB/c小鼠中,乳腺辐射刺激了癌细胞的侵袭,这与循环肿瘤细胞数量增加和肺转移有关。下调MT1-MMP可预防辐射的这些不良影响。
本研究表明,MT1-MMP是辐射增强肺转移发展所必需的,其表达水平和/或定位可作为预测一些TNBC患者早期复发的生物标志物进行评估。