Sun Yanqin, Yi Yanmei, Gan Siyuan, Ye Ruifang, Huang Cailing, Li Man, Huang Jian, Guo Ying
Department of Pathology, Guangdong Medical University, Dongguan, Guangdong 523808, P.R. China.
Center of Pathology Diagnosis and Research, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong 524023, P.R. China.
Oncol Lett. 2021 Jun;21(6):459. doi: 10.3892/ol.2021.12720. Epub 2021 Apr 8.
Numerous studies have suggested that non-coding RNAs mediate tumorigenesis via the epithelial-mesenchymal transition (EMT). However, whether the long non-coding RNA (lncRNA) HOXA transcript at the distal tip (HOTTIP) plays a role in the EMT of small cell lung cancer (SCLC) remains unclear. The results of the present study suggest that HOTTIP-knockdown may lead to a significant increase in E-cadherin expression and a decrease in vimentin (VIM) expression; these proteins are two key markers of EMT. Furthermore, a notable morphological change in SCLC cells with HOTTIP-knockdown was observed: After upregulation of microRNA (miR)-574-5p, the cells exhibited a long, fusiform morphology. Investigating these phenomena further revealed that HOTTIP may participate in EMT by binding to miR-574-5p. In addition, using bioinformatics technology and a dual luciferase reporter assay, it was found that miR-574-5p inhibited VIM expression via direct binding and interaction. In summary, the present results indicate that HOTTIP may be involved in the EMT of SCLC by binding to miR-574-5p, and that miR-574-5p may act through VIM, which is a key marker of EMT.
众多研究表明，非编码RNA通过上皮-间质转化（EMT）介导肿瘤发生。然而，远端HOXA转录本的长链非编码RNA（lncRNA）（HOTTIP）在小细胞肺癌（SCLC）的EMT中是否发挥作用仍不清楚。本研究结果表明，敲低HOTTIP可能导致E-钙黏蛋白表达显著增加，波形蛋白（VIM）表达减少；这些蛋白是EMT的两个关键标志物。此外，观察到敲低HOTTIP的SCLC细胞有明显的形态学变化：上调微小RNA（miR）-574-5p后，细胞呈现长梭形形态。对这些现象的进一步研究表明，HOTTIP可能通过与miR-574-5p结合参与EMT。此外，利用生物信息学技术和双荧光素酶报告基因检测发现，miR-574-5p通过直接结合和相互作用抑制VIM表达。总之，目前的结果表明，HOTTIP可能通过与miR-574-5p结合参与SCLC的EMT，并且miR-574-5p可能通过EMT的关键标志物VIM发挥作用。
