Wolf Katarina, Wu Yi I, Liu Yueying, Geiger Jörg, Tam Eric, Overall Christopher, Stack M Sharon, Friedl Peter
Rudolf Virchow Center, DFG Research Center for Experimental Biomedicine and Department of Dermatology, University of Würzburg, Josef-Schneider-Strasse 2, 97080 Würzburg, Germany.
Nat Cell Biol. 2007 Aug;9(8):893-904. doi: 10.1038/ncb1616. Epub 2007 Jul 8.
Invasive cell migration through tissue barriers requires pericellular remodelling of extracellular matrix (ECM) executed by cell-surface proteases, particularly membrane-type-1 matrix metalloproteinase (MT1-MMP/MMP-14). Using time-resolved multimodal microscopy, we show how invasive HT-1080 fibrosarcoma and MDA-MB-231 breast cancer cells coordinate mechanotransduction and fibrillar collagen remodelling by segregating the anterior force-generating leading edge containing beta1 integrin, MT1-MMP and F-actin from a posterior proteolytic zone executing fibre breakdown. During forward movement, sterically impeding fibres are selectively realigned into microtracks of single-cell calibre. Microtracks become expanded by multiple following cells by means of the large-scale degradation of lateral ECM interfaces, ultimately prompting transition towards collective invasion similar to that in vivo. Both ECM track widening and transition to multicellular invasion are dependent on MT1-MMP-mediated collagenolysis, shown by broad-spectrum protease inhibition and RNA interference. Thus, invasive migration and proteolytic ECM remodelling are interdependent processes that control tissue micropatterning and macropatterning and, consequently, individual and collective cell migration.
侵袭性细胞通过组织屏障迁移需要由细胞表面蛋白酶,特别是膜型-1基质金属蛋白酶(MT1-MMP/MMP-14)对细胞外基质(ECM)进行胞周重塑。利用时间分辨多模态显微镜,我们展示了侵袭性的HT-1080纤维肉瘤细胞和MDA-MB-231乳腺癌细胞如何通过将包含β1整合素、MT1-MMP和F-肌动蛋白的产生力的前沿与执行纤维分解的后蛋白水解区分开,来协调机械转导和纤维状胶原重塑。在向前运动过程中,空间上阻碍的纤维被选择性地重新排列成单细胞口径的微轨迹。微轨迹通过后续多个细胞对侧向ECM界面的大规模降解而扩大,最终促使向类似于体内的集体侵袭转变。ECM轨迹加宽和向多细胞侵袭的转变都依赖于MT1-MMP介导的胶原溶解,广谱蛋白酶抑制和RNA干扰表明了这一点。因此,侵袭性迁移和蛋白水解性ECM重塑是相互依存的过程,它们控制着组织微模式和大模式,进而控制个体和集体细胞迁移。