Department of Bioengineering, University of Illinois at Urbana Champaign, Urbana, Illinois.
Department of Materials Science and Engineering, University of Illinois at Urbana Champaign, Urbana, Illinois.
Mol Cancer Ther. 2018 Jan;17(1):119-129. doi: 10.1158/1535-7163.MCT-17-0070. Epub 2017 Nov 14.
Cancer stem cells are known to be controlled by pathways that are dormant in normal adult cells, for example, PTEN, which is a negative regulator of transcription factor STAT3. STAT3 regulates genes that are involved in stem cell self-renewal and thus represents a novel therapeutic target of enormous clinical significance. Studies on breast cancer stem cells (BCSC) have been also significantly correlated with STATs. We describe here for the first time a novel strategy to selectively target CSCs and to induce downregulation of STAT3 downstream target genes reducing expression of series of "stem-ness genes" in treated tumors. and experiments were performed to evaluate functional activity with gene and protein expression studies. The results of the study indicate that this targeted delivery approach deactivates STAT3 causing a reduction of CD44/CD24 CSC populations with aptly tracked gene and protein regulations of "stemness" characteristics. .
癌症干细胞被认为受正常成年细胞中休眠的通路所控制，例如，PTEN 是转录因子 STAT3 的负调节剂。STAT3 调节参与干细胞自我更新的基因，因此代表了具有巨大临床意义的新型治疗靶标。乳腺癌干细胞 (BCSC) 的研究也与 STATs 显著相关。我们在这里首次描述了一种新的策略，用于选择性靶向 CSCs 并诱导 STAT3 下游靶基因下调，从而降低治疗肿瘤中一系列“干性基因”的表达。进行了 和 实验来评估基因和蛋白质表达研究的功能活性。研究结果表明，这种靶向递药方法使 STAT3 失活，导致 CD44/CD24 CSC 群体减少，并且“干性”特征的基因和蛋白质调节得到适当跟踪。
