miR-125b、miR-100 和 miR-99a 共同调控儿童急性淋巴细胞白血病对长春新碱的耐药性。
MiR-125b, miR-100 and miR-99a co-regulate vincristine resistance in childhood acute lymphoblastic leukemia.
机构信息
Department of Pediatric Oncology and Hematology, Erasmus MC/Sophia Children's Hospital, University Medical Centre Rotterdam, Rotterdam, The Netherlands.
出版信息
Leuk Res. 2013 Oct;37(10):1315-21. doi: 10.1016/j.leukres.2013.06.027. Epub 2013 Jul 31.
MicroRNA-125b (miR-125b), miR-99a and miR-100 are overexpressed in vincristine-resistant acute lymphoblastic leukemia (ALL). Cellular viability of ETV6-RUNX1-positive Reh cells significantly increased in presence of 9 ng/mL vincristine upon co-expression of miR-125b/miR-99a (91 ± 4%), miR-125b/miR-100 (93 ± 5%) or miR-125b/miR-99a/miR-100 (82 ± 17%) compared with miR-125b-transduced cells (38 ± 13%, P<0.05). Co-expression of these miRNAs resulted in downregulation of DNTT, NUCKS1, MALAT1, SNRPE, PNO1, SET, KIF5B, PRPS2, RPS11, RPL38 and RPL23A (fold-change 1.3-1.9, p<0.05). Similarly, 7 out of these genes are lower expressed in vincristine-resistant ALL cells of children (p<0.05). The concerted function of miR-125b in combination with miR-99a and/or miR-100 illustrates the complexity of vincristine-resistant pediatric ALL.
微小 RNA-125b（miR-125b）、miR-99a 和 miR-100 在长春新碱耐药急性淋巴细胞白血病（ALL）中过表达。在共表达 miR-125b/miR-99a（91±4%）、miR-125b/miR-100（93±5%）或 miR-125b/miR-99a/miR-100（82±17%）时，ETV6-RUNX1 阳性 Reh 细胞的细胞活力在存在 9ng/mL 长春新碱的情况下显著增加与转染 miR-125b 的细胞（38±13%，P<0.05）相比。这些 miRNA 的共表达导致 DNTT、NUCKS1、MALAT1、SNRPE、PNO1、SET、KIF5B、PRPS2、RPS11、RPL38 和 RPL23A 的下调（倍数变化 1.3-1.9，p<0.05）。同样，这些基因中有 7 个在儿童长春新碱耐药 ALL 细胞中的表达较低（p<0.05）。miR-125b 与 miR-99a 和/或 miR-100 的协同作用说明了儿童长春新碱耐药性 ALL 的复杂性。
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