Department of General Surgery, Central South University, Changsha 410008, China
Cancer Invest. 2013 Jan;31(1):17-23. doi: 10.3109/07357907.2012.743557.
In this study, we investigated ALDH1A3, Mcl1, and miR-125a/b expression in HT29 cells and the effect of miR-125a/b on ALDH1A3 and Mcl1 expression. Our results showed that low expression of miR-125a/b and high expression of ALDH1A3 and Mel1 were observed in both ALDH1-positive HT29 and HT29-taxol cells. Overexpression of miR-125a/b significantly inhibited ALDH1A3 and Mcl1 expression, reduced cell survival, and increased cell apoptosis in HT29-taxol cells. Injection of miR-125a/b expression vector inhibited tumor growth in xenograft HT29-taxol mouse model. The current study suggested that miR-125a/b expression plays a key role in chemoresistance through upregulating ALDH1A3 and Mcl1 gene expression.
在这项研究中,我们研究了 ALDH1A3、Mcl1 和 miR-125a/b 在 HT29 细胞中的表达以及 miR-125a/b 对 ALDH1A3 和 Mcl1 表达的影响。我们的结果表明,ALDH1 阳性的 HT29 和 HT29-taxol 细胞中均观察到 miR-125a/b 表达降低和 ALDH1A3、Mcl1 表达升高。miR-125a/b 的过表达显著抑制了 HT29-taxol 细胞中 ALDH1A3 和 Mcl1 的表达,降低了细胞存活率,增加了细胞凋亡。miR-125a/b 表达载体的注射抑制了异种移植 HT29-taxol 小鼠模型中的肿瘤生长。本研究表明,miR-125a/b 表达通过上调 ALDH1A3 和 Mcl1 基因表达在化疗耐药中发挥关键作用。