1. Force-mediated proinvasive matrix remodeling driven by tumor-associated mesenchymal stem-like cells in glioblastoma
- Author
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Seok Gu Kang, Yongjoon Suh, Seungmo Kim, Eun Jung Lim, and Su Jae Lee
- Subjects
0301 basic medicine ,Myosin Light Chains ,Myosin light-chain kinase ,Stromal cell ,Tumor-associated mesenchymal stem-like cells ,Biochemistry ,Extracellular matrix ,03 medical and health sciences ,Cell Movement ,Cell Line, Tumor ,Tumor Microenvironment ,Humans ,Neoplasm Invasiveness ,Phosphorylation ,Molecular Biology ,Aged ,Tumor microenvironment ,Actomyosin contractility ,Janus kinase 1 ,Brain Neoplasms ,Chemistry ,Mesenchymal stem cell ,Mesenchymal Stem Cells ,Actomyosin ,Janus Kinase 1 ,Articles ,General Medicine ,Fibroblasts ,Extracellular Matrix ,Cell biology ,Proinvasive extracellular matrix remodeling ,030104 developmental biology ,Cell culture ,Cancer cell ,Neoplastic Stem Cells ,Female ,Glioblastoma ,Cardiac Myosins - Abstract
In carcinoma, cancer-associated fibroblasts participate in force-mediated extracellular matrix (ECM) remodeling, consequently leading to invasion of cancer cells. Likewise, the ECM remodeling actively occurs in glioblastoma (GBM) and the consequent microenvironmental stiffness is strongly linked to migration behavior of GBM cells. However, in GBM the stromal cells responsible for force-mediated ECM remodeling remain unidentified. We show that tumor-associated mesenchymal stem-like cells (tMSLCs) provide a proinvasive matrix condition in GBM by force-mediated ECM remodeling. Importantly, CCL2-mediated Janus kinase 1 (JAK1) activation increased phosphorylation of myosin light chain 2 in tMSLCs and led to collagen assembly and actomyosin contractility. Collectively, our findings implicate tMSLCs as stromal cells providing force-mediated proinvasive ECM remodeling in the GBM microenvironment, and reminiscent of fibroblasts in carcinoma. [BMB Reports 2018; 51(4): 182-187].
- Published
- 2018
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