Literature DB >> 23084187

Micro-RNA-21 regulates the sensitivity to cisplatin in human neuroblastoma cells.

Yun Chen1, Ya-Hui Tsai, Yu Fang, Sheng-Hong Tseng.   

Abstract

BACKGROUND/
PURPOSE: Drug resistance often causes treatment failure in neuroblastomas. Increasing evidence has implicated that the micro-RNAs (miRNAs) are involved in the development of drug resistance. In this report, we aimed to investigate the role of miRNA in cisplatin resistance of neuroblastoma cells.
MATERIALS AND METHODS: The cell viability of the neuroblastoma cells after cisplatin treatment was analyzed. The expression of the miRNAs and phosphatase and tensin homolog (PTEN) messenger RNA in the neuroblastoma cells was studied by real-time polymerase chain reaction. Overexpression of miRNA or suppression of miRNA expression by antagomir was used to investigate the effects of miRNA on the cisplatin-induced cell death or proliferation.
RESULTS: The expression of miR-21 was increased in the cisplatin-resistant (CisR) neuroblastoma cells as compared with the parental cells, and the antagomir against miR-21 converted the resistant cells into sensitive ones. Ectopic expression of pre-miR-21 in parental cells resulted in decreased sensitivity to cisplatin treatment. In addition, overexpression of pre-miR-21 markedly increa sed the proliferation rate of neuroblastoma cells. The level of PTEN messenger RNA and protein in the CisR cells was lower than that in the parental cells. Transfection of pre-miR-21 into the parental cells reduced the PTEN expression, and transfection of anti-miR-21 into the CisR cells increased the PTEN expression.
CONCLUSION: Micro-RNA-21 regulated the drug resistance and proliferation in neuroblastoma cells.
Copyright © 2012 Elsevier Inc. All rights reserved.

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Year:  2012        PMID: 23084187     DOI: 10.1016/j.jpedsurg.2012.05.013

Source DB:  PubMed          Journal:  J Pediatr Surg        ISSN: 0022-3468            Impact factor:   2.545


  20 in total

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10.  MicroRNA-21 promotes the ovarian teratocarcinoma PA1 cell line by sustaining cancer stem/progenitor populations in vitro.

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