■间变性甲状腺癌(ATC)是人类中最具侵袭性的恶性肿瘤之一,其与癌症相关的死亡率相当高。由于常规疗法缺乏足够的疗效,需要新的治疗方法。通过更好地了解ATC的分子发病机制可以实现这一目标。甲状腺肿瘤发生由称为癌症干细胞(CSC)的细胞亚群引发,所述细胞亚群具有赋予诸如自我更新和转移的过程的特定标志物诸如CD133。此外,一些长链非编码RNA(lncRNA)通过介导上述过程促进肿瘤发生。
■这里,我们设计了一项探索性研究来研究lncRNAsROR和MALAT1及其相关基因在CSC干性中的作用。使用磁激活细胞分选(MACS),在SW1736和C643ATC细胞系中分离CD133-和CD133+亚群。接下来,CD133标记的表达谱,MALAT1及其相关基因(CCND1,NESTIN,MYBL2,MCL1,IQGAP1),以及ROR及其相关基因(POU5F1,SOX2,NANOG),通过qRT-PCR进行了探索。
■我们发现ROR显著上调,POU5F1,SOX2,NANOG,CD133+SW1736细胞中的CD133、MALAT1、IQGAP1和MCL1与CD133-细胞比拟。至于CD133+C643细胞,CCND1,IQGAP1,POU5F1,SOX2,NANOG,与CD133-细胞相比,NESTIN显著上调。
■这项研究表明,CD133阳性SW1736和C643细胞中的这些lncRNAs可能调节ATC的干性行为。
UNASSIGNED: Anaplastic thyroid cancer (ATC) is one of the most aggressive malignancies in humans that accounts for a considerable rate of cancer-associated mortality. Since conventional therapies are lacking sufficient efficacy, new treatment approaches are required. This goal could be achieved through a better understanding of the molecular pathogenesis of ATC. Thyroid tumorigenesis is initiated by a subpopulation of cells known as cancer stem cells (CSCs) with specific markers such as CD133 that confers to processes such as self-renewal and metastasis. Besides, some long non-coding RNAs (lncRNAs) promote tumorigenesis by mediating the aforementioned processes.
UNASSIGNED: Here, we designed an exploratory
study to investigate the role of lncRNAs ROR and MALAT1 and their related genes in CSC stemness. Using magnetic-activated cell sorting (MACS), the CD133- and CD133+ subpopulations were separated in SW1736 and C643 ATC cell lines. Next, the expression profiles of the CD133 marker, MALAT1, and its associated genes (CCND1, NESTIN, MYBL2, MCL1, IQGAP1), as well as ROR and its related genes (POU5F1, SOX2, NANOG), were explored by qRT-PCR.
UNASSIGNED: We found significant up-regulation of ROR, POU5F1, SOX2, NANOG, CD133, MALAT1, IQGAP1, and MCL1 in CD133+ SW1736 cells compared to CD133- cells. As for CD133+ C643 cells, CCND1, IQGAP1, POU5F1, SOX2, NANOG, and NESTIN were significantly up-regulated compared to CD133- cells.
UNASSIGNED: This
study suggests that these lncRNAs in CD133-positive SW1736 and C643 cells might regulate stemness behaviors in ATC.