The Mechanical Rigidity of the Extracellular Matrix Regulates the Structure, Motility, and Proliferation of Glioma Cells

Theresa A. Ulrich, Elena M. De‐Juan‐Pardo, Sanjay Kumar

Cancer Research · 2009 · 891 citations · 42 references

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TL;DR

Glioblastoma multiforme is a highly aggressive astrocytoma with median survival of 15 months, whose rapid progression is driven in part by diffuse infiltration of single tumor cells that aberrantly interact with the extracellular matrix. The study tests whether mechanical cues from the extracellular matrix influence glioma cell properties that underlie invasion. Researchers cultured multiple glioma cell lines on fibronectin‑coated polymeric substrates of defined rigidity to examine how ECM stiffness affects cell structure, migration, and proliferation. Tumor cells spread, form stress fibers, and migrate rapidly on rigid ECM, but become rounded and non‑motile on compliant substrates, with proliferation similarly reduced; inhibition of nonmuscle myosin II abolishes this rigidity sensitivity, supporting a model where ECM stiffness regulates GBM invasiveness through actomyosin contractility.

Abstract

Glioblastoma multiforme (GBM) is a malignant astrocytoma of the central nervous system associated with a median survival time of 15 months, even with aggressive therapy. This rapid progression is due in part to diffuse infiltration of single tumor cells into the brain parenchyma, which is thought to involve aberrant interactions between tumor cells and the extracellular matrix (ECM). Here, we test the hypothesis that mechanical cues from the ECM contribute to key tumor cell properties relevant to invasion. We cultured a series of glioma cell lines (U373-MG, U87-MG, U251-MG, SNB19, C6) on fibronectin-coated polymeric ECM substrates of defined mechanical rigidity and investigated the role of ECM rigidity in regulating tumor cell structure, migration, and proliferation. On highly rigid ECMs, tumor cells spread extensively, form prominent stress fibers and mature focal adhesions, and migrate rapidly. As ECM rigidity is lowered to values comparable with normal brain tissue, tumor cells appear rounded and fail to productively migrate. Remarkably, cell proliferation is also strongly regulated by ECM rigidity, with cells dividing much more rapidly on rigid than on compliant ECMs. Pharmacologic inhibition of nonmuscle myosin II-based contractility blunts this rigidity-sensitivity and rescues cell motility on highly compliant substrates. Collectively, our results provide support for a novel model in which ECM rigidity provides a transformative, microenvironmental cue that acts through actomyosin contractility to regulate the invasive properties of GBM tumor cells.

References

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