Institute of Pathology, Hannover Medical School, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany.
Leuk Res. 2010 Mar;34(3):328-34. doi: 10.1016/j.leukres.2009.06.014. Epub 2009 Jul 16.
We investigated whether, in myelodysplastic syndromes (MDS), aberrant expression of miR-150/miR-221/miR-222 and their designated target mRNA molecules MYB, p27 and c-KIT may be involved in insufficient haematopoiesis. In a series of MDS (n=52), an aberrant increase of miR-150 was found only in MDS with associated del(5q) (n=9; p<0.01). The mRNA expression of transcription factor MYB, the designated target of miR-150, was shown to correlate inversely with the miR-150 level. Acute leukaemia evolving from MDS (n=11) showed significantly decreased levels of miR-221 but not miR-222. We conclude that inhibition of proliferation via over-expressed miR-150 might contribute to myelodysplastic haematopoiesis in MDS-del(5q).
我们研究了骨髓增生异常综合征(MDS)中,miR-150/miR-221/miR-222 的异常表达及其指定的靶分子 MYB、p27 和 c-KIT 是否与造血不足有关。在一系列 MDS(n=52)中,仅在伴有 del(5q)的 MDS 中发现 miR-150 异常增加(n=9;p<0.01)。miR-150 的指定靶基因转录因子 MYB 的 mRNA 表达与 miR-150 水平呈负相关。从 MDS 发展而来的急性白血病(n=11)显示 miR-221 水平显著降低,但 miR-222 水平没有降低。我们得出结论,通过过表达 miR-150 抑制增殖可能有助于 MDS-del(5q)中的骨髓增生异常造血。