MiR-29a-Mediated CD133 Expression Contributes to Cisplatin Resistance in CD133 Glioblastoma Stem Cells.

08:00 EDT 29th September 2018 | BioPortfolio

Summary of "MiR-29a-Mediated CD133 Expression Contributes to Cisplatin Resistance in CD133 Glioblastoma Stem Cells."

CD133 positive (CD133) cells are cancer stem cells in glioblastoma that are associated with poor prognosis and resistance to radiotherapy. However, the role of CD133 in chemoresistance is inconclusive, although recent studies suggest that increased CD133 expression may lead to increased cisplatin resistance under certain circumstances. In this study, we further explored the mechanism underlying CD133-mediated cisplatin resistance in glioblastoma stem cells. We sorted human glioblastoma T98G and U87MG cells into CD133 and CD133 pools and measured apoptosis and CD133 expression levels in response to cisplatin treatment. We predicted candidate microRNAs that might target CD133 and assessed their levels in cisplatin-treated CD133 cells. Finally, we overexpressed miR-29a in CD133 cells and tested its effects in cisplatin-mediated apoptosis and survival of CD133 tumor bearing mice receiving cisplatin treatment. We found that CD133 glioblastoma stem cells showed more resistance to cisplatin treatment. Cisplatin increased CD133 expression by suppressing miR-29a levels. MiR-29a overexpression improved sensitivity of cisplatin in CD133 cells and significantly suppressed tumor growth in CD133 tumor bearing mice in response to cisplatin treatment. Our data show that miR-29a ameliorates CD133-mediated chemoresistance in glioblastoma stem cells, suggesting it as a potential therapeutic target for treating glioblastoma.


Journal Details

This article was published in the following journal.

Name: Journal of molecular neuroscience : MN
ISSN: 1559-1166


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Medical and Biotech [MESH] Definitions

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A catalytic subunit of the NuA4 histone acetyltransferase complex that functions in transcriptional activation of genes by acetylation of nucleosomal HISTONES H4 and H2A, altering nucleosome-DNA interactions and interaction of the modified histones with other activating transcription factors. It may control gene expression changes associated with oncogene and proto-oncogene mediated growth induction, tumor suppressor mediated growth arrest; CELL AGING; APOPTOSIS; and DNA REPAIR. It is polyubiquitinated and degraded during HIV-1 infection through its interaction with the viral TAT PROTEIN.

An ATP binding cassette transporter, sub-family G protein that functions as a high capacity UREA exporter, transporter of STEROLS, and in the absorption and efflux of many drugs. Its efflux activity for ANTINEOPLASTIC AGENTS contributes to DRUG RESISTANCE. It functions as a homodimer and is expressed by cells in a variety of organs, as well as by NEOPLASTIC STEM CELLS.

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