当前位置:
X-MOL 学术
›
Mol. Cancer Ther.
›
论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Targeted Delivery of STAT-3 Modulator to Breast Cancer Stem Like Cells Down-regulates a Series of Stem-ness Genes
Molecular Cancer Therapeutics ( IF 5.7 ) Pub Date : 2017-11-14 , DOI: 10.1158/1535-7163.mct-17-0070 Santosh K Misra 1, 2, 3 , Arun De 1, 2, 3 , Dipanjan Pan 1, 2, 3
Molecular Cancer Therapeutics ( IF 5.7 ) Pub Date : 2017-11-14 , DOI: 10.1158/1535-7163.mct-17-0070 Santosh K Misra 1, 2, 3 , Arun De 1, 2, 3 , Dipanjan Pan 1, 2, 3
Affiliation
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. In vitro and in vivo 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. Mol Cancer Ther; 17(1); 119–29. ©2017 AACR.
中文翻译:
将 STAT-3 调节剂靶向递送至乳腺癌干细胞样细胞可下调一系列干细胞基因
已知癌症干细胞受在正常成体细胞中休眠的通路控制,例如 PTEN,它是转录因子 STAT3 的负调节因子。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点。对乳腺癌干细胞 (BCSC) 的研究也与 STAT 显着相关。我们在此首次描述了一种选择性靶向 CSC 并诱导 STAT3 下游靶基因下调的新策略,从而降低治疗肿瘤中一系列“干性基因”的表达。进行体外和体内实验以评估基因和蛋白质表达研究的功能活性。研究结果表明,这种靶向递送方法使 STAT3 失活,导致 CD44+/CD24- CSC 种群减少,具有适当追踪的“干性”特征的基因和蛋白质调节。摩尔癌症治疗;17(1);119–29。©2017 AACR。
更新日期:2017-11-14
中文翻译:
将 STAT-3 调节剂靶向递送至乳腺癌干细胞样细胞可下调一系列干细胞基因
已知癌症干细胞受在正常成体细胞中休眠的通路控制,例如 PTEN,它是转录因子 STAT3 的负调节因子。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点。对乳腺癌干细胞 (BCSC) 的研究也与 STAT 显着相关。我们在此首次描述了一种选择性靶向 CSC 并诱导 STAT3 下游靶基因下调的新策略,从而降低治疗肿瘤中一系列“干性基因”的表达。进行体外和体内实验以评估基因和蛋白质表达研究的功能活性。研究结果表明,这种靶向递送方法使 STAT3 失活,导致 CD44+/CD24- CSC 种群减少,具有适当追踪的“干性”特征的基因和蛋白质调节。摩尔癌症治疗;17(1);119–29。©2017 AACR。