H Gao1, J-Y Yang, L-X Tong, H Jin, C-Z Liu. 1. Department of Thyroid Head and Neck Surgery, Tumor Hospital of Jinlin Province, Changchun, China. zfzf1997@126.com.
Abstract
OBJECTIVE: Recently, long noncoding RNAs (lncRNAs) have attracted much attention for their roles in tumor progression. The aim of this study was to investigate the exact role of lncRNA UCA1 in the development of thyroid cancer (TC) and to explore the possible underlying mechanism. PATIENTS AND METHODS: UCA1 expression in both TC cells and tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Colony formation assay, cell proliferation, and transwell assay were conducted in vitro. Subsequent luciferase reporter gene assay was applied to investigate the underlying mechanism. Furthermore, the function of UCA1 in vivo was monitored as well. RESULTS: UCA1 expression level in TC samples was significantly higher than that of corresponding normal tissues. After UCA1 was knocked down in vitro and in vivo, the proliferation, migration, and invasion of TC cells were significantly inhibited. Moreover, the expression of miR-497-3p was repressed after the knockdown of UCA1. Furthermore, miR-497-3p was directly targeted by UCA1. CONCLUSIONS: Knockdown of UCA1 could inhibit TC cell proliferation and metastasis via sponging miR-497-3p. Our findings might offer a new therapeutic intervention for TC patients.
OBJECTIVE: Recently, long noncoding RNAs (lncRNAs) have attracted much attention for their roles in tumor progression. The aim of this study was to investigate the exact role of lncRNA UCA1 in the development of thyroid cancer (TC) and to explore the possible underlying mechanism. PATIENTS AND METHODS: UCA1 expression in both TC cells and tissues was detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Colony formation assay, cell proliferation, and transwell assay were conducted in vitro. Subsequent luciferase reporter gene assay was applied to investigate the underlying mechanism. Furthermore, the function of UCA1 in vivo was monitored as well. RESULTS:UCA1 expression level in TC samples was significantly higher than that of corresponding normal tissues. After UCA1 was knocked down in vitro and in vivo, the proliferation, migration, and invasion of TC cells were significantly inhibited. Moreover, the expression of miR-497-3p was repressed after the knockdown of UCA1. Furthermore, miR-497-3p was directly targeted by UCA1. CONCLUSIONS: Knockdown of UCA1 could inhibit TC cell proliferation and metastasis via sponging miR-497-3p. Our findings might offer a new therapeutic intervention for TCpatients.