Abstract
Selective inhibition of BCR/ABL expression by RNA interference has been demonstrated as an effective strategy in CML treatment and a reversal to imatinib resistance. microRNAs (miRNAs) are small regulatory RNAs involved in post-transcriptional gene regulation. miR-203 is supposed to directly regulate ABL and BCR/ABL expression, however, the role of miR-203 in imatinib-resistant cells is not clear. Here, we report that overexpression of miR-203 in BaF3-BCR/ABL cells with T315I mutant inhibited cell growth and colony formation ability. Furthermore, miR-203 increased sensitivity to imatinib in BaF3-BCR/ABL(T315I) cells, thereby antagonizing the main mechanism of resistance to imatinib.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adult
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Animals
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Benzamides / pharmacology*
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Blotting, Western
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Cell Cycle / drug effects
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Cell Cycle / genetics
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Cell Proliferation / drug effects
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Female
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Fusion Proteins, bcr-abl / genetics
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Fusion Proteins, bcr-abl / metabolism*
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Humans
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Imatinib Mesylate
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Male
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Mice
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MicroRNAs / genetics
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MicroRNAs / metabolism*
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Middle Aged
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Piperazines / pharmacology*
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Pyrimidines / pharmacology*
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Reverse Transcriptase Polymerase Chain Reaction
Substances
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Benzamides
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MIRN203 microRNA, human
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MicroRNAs
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Piperazines
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Pyrimidines
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Imatinib Mesylate
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Fusion Proteins, bcr-abl
Grants and funding
This work was supported by the Doctor Foundation of school of Medical Lab Science, Chongqing Medical University to Yajuan Li. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.