CircRANBP17 modulated KDM1A to regulate neuroblastoma progression by sponging miR-27b-3p

Author:

Zhao Lijun1,Fan Junying2,Zhang Chunyang3,Zhang Zhenjun3,Dong Jun4

Affiliation:

1. Department of Neurosurgery, The Second Affiliated Hospital of Soochow University , Suzhou City , Jiangsu Province, 215000 , China

2. Department of Nephrology, The First Affiliated Hospital of Baotou Medical College , Baotou , China

3. Department of Neurosurgery, The First Affiliated Hospital of Baotou Medical College , Baotou , China

4. Department of Neurosurgery, The Second Affiliated Hospital of Soochow University , No. 1055, Sanxiang Road, Gusu District , Suzhou City , Jiangsu Province, 215000 , China

Abstract

Abstract Neuroblastoma (NB) is a common childhood cancer. Circular RNA RAN binding protein 17 (circRANBP17) has been identified to participate in diverse tumor progression. This study aims to explore the function and mechanism of circRANBP17 in NB. The levels of circRANBP17, miR-27b-3p and KDM1A in NB tissues and cells were measured by qRT-PCR. Mouse model assay was performed to investigate the effect of circRANBP17 knockdown on tumor formation in vivo. The levels of circRANBP17 and KDM1A were significantly up-regulated, and the level of miR-27b-3p was strikingly down-regulated in NB tissues and cells (SK-N-SH and SK-N-AS). Functional studies indicated that miR-27b-3p inhibitor mitigated the inhibitory effects on cell proliferation, migration, invasion and the promoting effect on cell apoptosis in SK-N-SH and SK-N-AS cells induced by circRANBP17 knockdown. Also, miR-27b-3p regulated NB cell malignancy by targeting KDM1A. Further studies revealed that miR-27b-3p inhibitor reversed the low expression of KDM1A induced by circRANBP17 knockdown. In support, circRANBP17 knockdown led to inhibition of tumor formation in vivo. In conclusion, circRANBP17 modulated KDM1A to promote cell proliferation, migration, invasion and restrain cell apoptosis in NB by sponging miR-27b-3p, and the new regulatory network may provide a theoretical basis for the further study of NB.

Publisher

Walter de Gruyter GmbH

Subject

General Medicine

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