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多步骤细胞周缘蛋白水解作用控制着癌细胞从个体侵袭向集体侵袭的转变。

Multi-step pericellular proteolysis controls the transition from individual to collective cancer cell invasion.

作者信息

Wolf Katarina, Wu Yi I, Liu Yueying, Geiger Jörg, Tam Eric, Overall Christopher, Stack M Sharon, Friedl Peter

机构信息

Rudolf Virchow Center, DFG Research Center for Experimental Biomedicine and Department of Dermatology, University of Würzburg, Josef-Schneider-Strasse 2, 97080 Würzburg, Germany.

出版信息

Nat Cell Biol. 2007 Aug;9(8):893-904. doi: 10.1038/ncb1616. Epub 2007 Jul 8.

Abstract

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.

摘要

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。

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