Correction of Bcl-x splicing improves responses to imatinib in chronic myeloid leukaemia cells and mouse models.
作者： Jing Zhang , Yan Wang , Shu‐Qi Li , Le Fang , Xiao‐Zhong Wang
DOI: 10.1111/BJH.16472
关键词: RNA splicing 、 Apoptosis 、 Flow cytometry 、 Imatinib mesylate 、 K562 cells 、 Cell culture 、 Imatinib 、 Biology 、 Cancer research 、 Viability assay
摘要: Imatinib mesylate (IM) resistance has become a major clinical problem for chronic myeloid leukaemia (CML). It is known that Bcl-x splicing deregulated and involved in multiple malignant cancer initiation chemotherapy resistance, including CML. The aim of the present study was to correct abnormal CML investigate subsequent phenotype changes, especially response IM. aberrant cells effectively restored using vivo-Morpholino Antisense Oligomer (vMO). CCK-8 cell viability assay flow cytometry showed restoring increases IM-induced growth inhibition apoptosis K562 cells. Moreover, more significant similar phenomenon observed imatinib-resistant lines K562/G01. Finally, establishment xenograft model had also proved correcting vivo can enhance anti-tumor effect Our findings suggest vMO co-operating with IM increase sensitivity both vitro vivo, could good candidates chemotherapy-sensitized target IM-resistant
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