Inhibition of BCR/ABL Protein Expression by miR-203 Sensitizes for Imatinib Mesylate
Yajuan Li, Ying Yuan, Kun Tao, Xin Wang, Qing Xiao, Zhenglan Huang, Liang Zhong, Weixi Cao, Jianping Wen, Wenli Feng
Abstract
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Yajuan Li, Ying Yuan, Kun Tao, Xin Wang, Qing Xiao, Zhenglan Huang, Liang Zhong, Weixi Cao, Jianping Wen, Wenli Feng
Abstract
Open-access reader
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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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.
Key concepts: Imatinib mesylate, Imatinib, breakpoint cluster region, RNA interference, ABL, microRNA, Cancer research, K562 cells