MicroRNA-93 promotes cell growth and invasion in nasopharyngeal carcinoma by targeting disabled homolog-2. Issue 2 (28th July 2015)

• Record Type: Journal Article
• Authors: Xu, Ya-Fei; Mao, Yan-Ping; Li, Ying-Qin; Ren, Xian-Yue; He, Qing-Mei; Tang, Xin-Ran; Sun, Ying; Liu, Na; Ma, Jun
• Is Part Of: Cancer letters. Volume 363:Issue 2(2015)
• Page Start: 146
• Page End: 155
• Publication Date: 2015-07-28
• Subjects: Nasopharyngeal carcinoma -- MiR-93 -- Dab2 -- Cell growth -- Invasion; Cancer -- Periodicals; Neoplasms -- Periodicals; Cancer -- Périodiques; Electronic journals; 616.994
• DOI: 10.1016/j.canlet.2015.04.006
• Languages: English
• ISSNs: 0304-3835

Abstract

Highlights: MiR-93 is upregulated in nasopharyngeal carcinoma cell lines and clinical tissues. Inhibition of miR-93 suppresses NPC cell growth, invasion and migration in vitro . Depletion of miR-93 suppresses NPC tumor growth in vivo . Disabled homolog-2 (Dab2) is verified as a miR-93 target gene. Dab2 was involved in miR-93-regulated NPC cell growth, invasion and migration. Abstract: Dysregulation of microRNAs (miRNAs) has been demonstrated to contribute to malignant progression in nasopharyngeal carcinoma (NPC). We previously reported that miR-93 was significantly upregulated in NPC based on a microarray analysis. However, the potential role and mechanism of action of miR-93 in the initiation and progression of NPC remain largely unknown. Quantitative RT-PCR demonstrated that miR-93 was significantly upregulated in NPC cell lines and clinical specimens. The MTT assay, colony formation assay, anchorage-independent growth, and Transwell migration and invasion assays showed that depletion of miR-93 inhibited NPC cell growth, invasion and migration in vitro and suppressed tumor growth in vivo . Disabled homolog-2 ( Dab2 ) was verified as a miR-93 target gene using Luciferase reporter assays, quantitative RT-PCR and Western blotting and was involved in miR-93-regulated NPC cell growth, invasion and migration. These results indicated that miR-93 plays an important role in the initiation and progression of NPC by targeting Dab2 and the miR-93/ Dab2 pathway may contribute to the development of novel therapeutic strategies for NPC in the future.