Ying Li1, Ya M Shang, Qi W Wang. 1. Department of Pediatrics, Huaihe Hospital of HeNan University, Kaifeng, Henan Province, China - xfzhang1982@sina.com.
Abstract
BACKGROUND: Neuroblastoma (NB) is one of the most common solid tumors in infants and children. Numerous reports demonstrated that microRNAs (miRNAs) play important roles in the carcinogenesis of neuroblastoma. miR-21 functions as a tumor oncogene in some malignancies. However, its role in NB remains poorly understood. METHODS: miR-21 expression was quantified in NB tissues and matched adjacent non-tumor tissues using quantitative real-time PCR (RT-PCR). Cell proliferation, migration, and invasion were measured following overexpression of miR-21 expression by miR-21 mimics. miR-21 targets were scanned using target prediction programs. Following the overexpression of miR-21, target gene expression was detected by western blotting. In addition, cell proliferation, migration, and invasion were measured following inhibition of CHL1 expression by siRNA. RESULTS: In the present study, our results showed that miR-21 was increased in NB tissues compared with matched adjacent non-tumor tissues. Forced overexpression of miR-21 significantly increased NB cell proliferation, migration, and invasion. Close homolog of LI (CHL1) was found to be a target of miR-21. Furthermore, downregulation of CHL1 by siRNA performed similar effects with overexpression of miR-21 in NB cells. CONCLUSIONS: We suggested that miR-21 promoted neuroblastoma cell growth and motility partially by targeting CHL1, indicating the potential utility of miR-21 inhibition as a novel therapeutic strategy against neuroblastoma.
BACKGROUND:Neuroblastoma (NB) is one of the most common solid tumors in infants and children. Numerous reports demonstrated that microRNAs (miRNAs) play important roles in the carcinogenesis of neuroblastoma. miR-21 functions as a tumor oncogene in some malignancies. However, its role in NB remains poorly understood. METHODS:miR-21 expression was quantified in NB tissues and matched adjacent non-tumor tissues using quantitative real-time PCR (RT-PCR). Cell proliferation, migration, and invasion were measured following overexpression of miR-21 expression by miR-21 mimics. miR-21 targets were scanned using target prediction programs. Following the overexpression of miR-21, target gene expression was detected by western blotting. In addition, cell proliferation, migration, and invasion were measured following inhibition of CHL1 expression by siRNA. RESULTS: In the present study, our results showed that miR-21 was increased in NB tissues compared with matched adjacent non-tumor tissues. Forced overexpression of miR-21 significantly increased NB cell proliferation, migration, and invasion. Close homolog of LI (CHL1) was found to be a target of miR-21. Furthermore, downregulation of CHL1 by siRNA performed similar effects with overexpression of miR-21 in NB cells. CONCLUSIONS: We suggested that miR-21 promoted neuroblastoma cell growth and motility partially by targeting CHL1, indicating the potential utility of miR-21 inhibition as a novel therapeutic strategy against neuroblastoma.