Lin Xiaojie, Guan Hongyu, Li Hai, Liu Liehua, Liu Juan, Wei Guohong, Huang Zhimin, Liao Zhihong, Li Yanbing
Department of Endocrinology and Diabetes Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510080, P.R. China.
Biomed Rep. 2014 Jan;2(1):122-126. doi: 10.3892/br.2013.192. Epub 2013 Oct 31.
Accumulating evidence suggests that some microRNAs (miRNAs) are involved in papillary thyroid carcinoma (PTC) progression. However, it remains necessary to elucidate the underlying molecular mechanisms involved. In the present study, we investigated the role of microRNA-101 (miR-101) in PTC via targeting of Ras-related C3 botulinum toxin substrate 1 (Rac1). The results showed that miR-101 was significantly downregulated in PTC tissues compared with adjacent normal tissues. Restoration of miR-101 expression significantly inhibited cell proliferation in the K1 PTC cell line. Moreover, algorithm-based and experimental strategies verified Rac1 as a direct target of miR-101 in the K1 cell line. Taken together, these findings suggest that miR-101 inhibited PTC growth via the downregulation of Rac1 expression, providing a better understanding of miRNA-modulated signaling networks for future cancer therapeutics.
越来越多的证据表明,一些微小RNA(miRNA)参与了甲状腺乳头状癌(PTC)的进展。然而,仍有必要阐明其中潜在的分子机制。在本研究中,我们通过靶向Ras相关的C3肉毒杆菌毒素底物1(Rac1)来研究微小RNA-101(miR-101)在PTC中的作用。结果显示,与相邻正常组织相比,miR-101在PTC组织中显著下调。miR-101表达的恢复显著抑制了K1 PTC细胞系中的细胞增殖。此外,基于算法和实验的策略证实Rac1是K1细胞系中miR-101的直接靶点。综上所述,这些发现表明miR-101通过下调Rac1表达来抑制PTC生长,为未来癌症治疗中miRNA调节的信号网络提供了更好的理解。