Inhibition of BCR/ABL Protein Expression by miR-203 Sensitizes for Imatinib Mesylate

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 regulat...

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Autores principales: Li, Yajuan, Yuan, Ying, Tao, Kun, Wang, Xin, Xiao, Qing, Huang, Zhenglan, Zhong, Liang, Cao, Weixi, Wen, Jianping, Feng, Wenli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2013
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3627914/
https://www.ncbi.nlm.nih.gov/pubmed/23613955
http://dx.doi.org/10.1371/journal.pone.0061858
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author Li, Yajuan
Yuan, Ying
Tao, Kun
Wang, Xin
Xiao, Qing
Huang, Zhenglan
Zhong, Liang
Cao, Weixi
Wen, Jianping
Feng, Wenli
author_facet Li, Yajuan
Yuan, Ying
Tao, Kun
Wang, Xin
Xiao, Qing
Huang, Zhenglan
Zhong, Liang
Cao, Weixi
Wen, Jianping
Feng, Wenli
author_sort Li, Yajuan
collection PubMed
description 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.
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spelling pubmed-36279142013-04-23 Inhibition of BCR/ABL Protein Expression by miR-203 Sensitizes for Imatinib Mesylate Li, Yajuan Yuan, Ying Tao, Kun Wang, Xin Xiao, Qing Huang, Zhenglan Zhong, Liang Cao, Weixi Wen, Jianping Feng, Wenli PLoS One Research Article 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. Public Library of Science 2013-04-16 /pmc/articles/PMC3627914/ /pubmed/23613955 http://dx.doi.org/10.1371/journal.pone.0061858 Text en © 2013 Li et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Li, Yajuan
Yuan, Ying
Tao, Kun
Wang, Xin
Xiao, Qing
Huang, Zhenglan
Zhong, Liang
Cao, Weixi
Wen, Jianping
Feng, Wenli
Inhibition of BCR/ABL Protein Expression by miR-203 Sensitizes for Imatinib Mesylate
title Inhibition of BCR/ABL Protein Expression by miR-203 Sensitizes for Imatinib Mesylate
title_full Inhibition of BCR/ABL Protein Expression by miR-203 Sensitizes for Imatinib Mesylate
title_fullStr Inhibition of BCR/ABL Protein Expression by miR-203 Sensitizes for Imatinib Mesylate
title_full_unstemmed Inhibition of BCR/ABL Protein Expression by miR-203 Sensitizes for Imatinib Mesylate
title_short Inhibition of BCR/ABL Protein Expression by miR-203 Sensitizes for Imatinib Mesylate
title_sort inhibition of bcr/abl protein expression by mir-203 sensitizes for imatinib mesylate
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3627914/
https://www.ncbi.nlm.nih.gov/pubmed/23613955
http://dx.doi.org/10.1371/journal.pone.0061858
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