JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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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.

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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