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Adipose-derived mesenchymal stem cells -conditioned medium effects on Glioma U87 cell line migration, apoptosis, and gene expression

The conditioned medium of mesenchymal stem cells (MSCs) has controversial roles in cancer, either promoting or suppressing tumor growth. Our research on the results of adipose tissue-derived MSC (AD-MSC)-conditioned media on U87 glioma cells was motivated by the disputed role of mesenchymal stem cel...

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Published in:Tissue & cell 2023-12, Vol.85, p.102224-102224, Article 102224
Main Authors: Jafari, Sorush, Hamidian, Marziye, Dashtaki, Masoumeh Eliyasi, Barzegar, Ali, Ghasemi, Sorayya
Format: Article
Language:English
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Summary:The conditioned medium of mesenchymal stem cells (MSCs) has controversial roles in cancer, either promoting or suppressing tumor growth. Our research on the results of adipose tissue-derived MSC (AD-MSC)-conditioned media on U87 glioma cells was motivated by the disputed role of mesenchymal stem cells (MSCs) in cancer, which may either promote or inhibit tumor growth. Using flow cytometry, AD-MSCs were identified, verified, and their conditioned media was used to treat U87 cells. Through RT-qPCR, scratch assay, and apoptosis analysis, we evaluated gene expression (SOX4, H19, and CCAT1), cell migration, and apoptosis in U87 cells.The conditioned media greatly increased the expression of SOX4 and H19, but not CCAT1. Although there were few differences in migration and apoptosis, both were slightly increased in the treated group.These outcomes have drawn attention to the complexity of the interactions between MSCs and glioma cells. This complexity requires further research to identify the specific mechanisms governing MSC-mediated impacts on the development of glioblastoma multiforme (GBM). [Display omitted] •The study examined the impact of AD-MSC-conditioned medium on U87 cells.•AD-MSC-conditioned medium increased SOX4 and H19 expression in U87 cells.•AD-MSC-conditioned medium did not affect apoptosis and cell migration.•Further research is essential for therapeutic strategies for GBM.
ISSN:0040-8166
1532-3072
DOI:10.1016/j.tice.2023.102224