Institute of Genetic Engineering, Southern Medical University, Guangzhou, China.
Leuk Res. 2013 Mar;37(3):349-56. doi: 10.1016/j.leukres.2012.12.003. Epub 2013 Jan 1.
Chronic myeloid leukemia (CML) is associated with overexpression of BCR-ABL1, a nonreceptor tyrosine kinase critical for malignant transformation. We investigated whether non-coding microRNAs (miRNAs) targeting BCR-ABL1 mRNA contribute to the pathogenesis of CML. Indeed, miR-30a targeted BCR-ABL1 and was underexpressed in bone marrow from CML patients. In K562 leukemia cells, overexpression of miR-30a reduced ABL1 and BCR-ABL1 protein expression, decreased proliferation, and arrested cell cycle progression between G1 and S. These findings strongly suggest that miR-30a acts as a tumor suppressor by downregulating ABL1 and BCR-ABL1 expression. Upregulation of miR-30a in hematopoietic cells may have therapeutic efficacy against CML.
慢性髓性白血病（CML）与 BCR-ABL1 的过度表达有关，BCR-ABL1 是一种非受体酪氨酸激酶，对恶性转化至关重要。我们研究了针对 BCR-ABL1 mRNA 的非编码 microRNAs（miRNAs）是否有助于 CML 的发病机制。事实上，miR-30a 靶向 BCR-ABL1，在 CML 患者的骨髓中表达下调。在 K562 白血病细胞中，miR-30a 的过表达降低了 ABL1 和 BCR-ABL1 蛋白的表达，减少了增殖，并阻止了细胞周期从 G1 到 S 的进展。这些发现强烈表明，miR-30a 通过下调 ABL1 和 BCR-ABL1 的表达发挥肿瘤抑制作用。造血细胞中 miR-30a 的上调可能对 CML 具有治疗效果。
