ArticleJournal of molecular neuroscience : MN2012
Glioma cells promote the expression of vascular cell adhesion molecule-1 on bone marrow-derived mesenchymal stem cells: a possible mechanism for their tropism toward gliomas.
Article in Journal of molecular neuroscience : MN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Mesenchymal stem cell-derived exosomes as new tools for delivery of miRNAs in the treatment of cancer.Frontiers in bioengineering and biotechnology · 2022Review
- Stem cells: a promising candidate to treat neurological disorders.Neural regeneration research · 2018Review
- Review
- Mesenchymal stromal cells (MSCs) and colorectal cancer: a troublesome twosome for the anti-tumour immune response?Oncotarget · 2016Review
- CD44 promotes the migration of bone marrow-derived mesenchymal stem cells toward glioma.Oncology letters · 2016Article
- CXCR4 receptor overexpression in mesenchymal stem cells facilitates treatment of acute lung injury in rats.The Journal of biological chemistry · 2015Article
- The roles of mesenchymal stem cells in tumor inflammatory microenvironment.Journal of hematology & oncology · 2014Review
- Article
- Vascular endothelial growth factor participates in modulating the C6 glioma-induced migration of rat bone marrow-derived mesenchymal stem cells and upregulates their vascular cell adhesion molecule-1 expression.Experimental and therapeutic medicine · 2012Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tropism of bone marrow-derived mesenchymal stem cells (BMSCs) toward gliomas has been shown by in vitro and in vivo assays. This study was carried out to evaluate the role of vascular cell adhesion molecule-1 (VCAM-1) in the migration of BMSCs towards glioma and the effect of glioma cells on the VCAM-1 expression of BMSCs. BMSCs were isolated according to their adherence to plastic. The tropism of BMSCs toward C6 and U87 glioma and the role of VCAM-1 in this migration were analyzed by in vitro migration assay, separately. Reverse transcription-polymerase chain reaction, immunofluorescence, and Western blot were employed to assess VCAM-1 expression of BMSCs when they were incubated by the conditioned mediums (CM) of C6 or U87 glioma cells. Data revealed that C6 and U87 glioma cells promote the migration of BMSCs, which could be blocked by a VCAM-1-neutralizing antibody. Moreover, VCAM-1 expression of BMSCs was elevated by the incubation of their CM. The results also demonstrated that LY294002, an inhibitor of phosphoinositide-3-kinase (PI3K), significantly inhibited the glioma-induced upregulation of VCAM-1 on BMSCs. These findings suggested that glioma-induced change in VCAM-1 expression of BMSCs may play an important role in their tropism towards glioma, and PI3K is associated with the signal transduction of this process.
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