ArticleFEBS open bio2018
Matrix metalloproteinase-1 facilitates MSC migration via cleavage of IGF-2/IGFBP2 complex.
Article in FEBS open bio, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Human Embryonic Stem Cell-Derived Immunity-And-Matrix-Regulatory Cells Attenuate Pulmonary Fibrosis via MMP1-Mediated Collagen Degradation.Cell proliferation · 2026Article
- Integration of Gastric Cancer RNA-Seq Datasets Along With PPI Network Suggests That Nonhub Nodes Have the Potential to Become Biomarkers.Cancer reports (Hoboken, N.J.) · 2025Article
- Harnessing the Therapeutic Potential of Mesenchymal Stem Cells in Cancer Treatment.Advanced pharmaceutical bulletin · 2024Review
- Dental pulp mesenchymal stem cells-response to fibrin hydrogel reveals ITGA2 and MMPs expression.Heliyon · 2024Article
- Tumor-tropic Trojan horses: Using mesenchymal stem cells as cellular nanotheranostics.Theranostics · 2024Review
- Subcellular mechano-regulation of cell migration in confined extracellular microenvironment.Biophysics reviews · 2023Review
- Effect of Expansion Media on Functional Characteristics of Bone Marrow-Derived Mesenchymal Stromal Cells.Cells · 2023Article
- Enhanced tumor targeting and timely viral release of mesenchymal stem cells/oncolytic virus complex due to GRP78 and inducible E1B55K expressions greatly increase the antitumor effect of systemic treatment.Molecular therapy oncolytics · 2022Article
- Manufacturing of primed mesenchymal stromal cells for therapy.Nature biomedical engineering · 2019Review
- Mesenchymal Stem Cell Migration during Bone Formation and Bone Diseases Therapy.International journal of molecular sciences · 2018Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The specific mechanism underlying the tumor tropism of human mesenchymal stem cells (MSCs) for cancer is not well defined. We previously showed that the migration potential of MSCs correlated with the expression and protease activity of matrix metalloproteinase (MMP)-1. Furthermore, highly tumor-tropic MSCs expressed higher levels of MMP-1 and insulin-like growth factor (IGF)-2 than poorly migrating MSCs. In this study, we examined the functional roles of IGF-2 and MMP-1 in mediating the tumor tropism of MSCs. Exogenous addition of either recombinant IGF-2 or MMP-1 could stimulate MSC migration. The correlation between IGF-2, MMP-1 expression, and MSC migration suggests that MMP-1 may play a role in regulating MSC migration via the IGF-2 signaling cascade. High concentrations of IGF binding proteins (IGFBPs) can inhibit IGF-stimulated functions by blocking its binding to its receptors and proteolysis of IGFBP is an important mechanism for the regulation of IGF signaling. We thus hypothesized that MMP-1 acts as an IGFBP2 proteinase, resulting in the cleavage of IGF-2/IGFBP2 complex and extracellular release of free IGF-2. Indeed, our results showed that conditioned media from highly migrating MSCs, which expressed high levels of MMP-1, cleaved the IGF-2/IGFBP2 complex. Taken together, these results showed that the MMP-1 secreted by highly tumor-tropic MSCs cleaved IGF-2/IGFBP2 complex. Free IGF-2 released from the complex may facilitate MSC migration toward tumor.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.