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Silencing of long non‐coding RNA DLX6‐AS1 weakens neuroblastoma progression by the miR ‐513c‐5p/ PLK4 axis
Author(s) -
Jia Peisheng,
Wei Erhu,
Liu Huiqiong,
Wu Tingting,
Wang Huaili
Publication year - 2020
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1002/iub.2392
Subject(s) - gene silencing , long non coding rna , antisense rna , microbiology and biotechnology , downregulation and upregulation , cancer research , chemistry , rna , biology , gene , biochemistry
Emerging evidence has demonstrated the crucial roles of long noncoding RNAs in human cancers, including neuroblastoma (NB). DLX6 antisense RNA 1 (DLX6‐AS1) has been identified as an oncogenic driver in NB. However, the mechanisms of DLX6‐AS1 in NB progression are not fully understood. Our data showed that DLX6‐AS1 was significantly overexpressed in NB tissues and cells. Moreover, DLX6‐AS1 silencing repressed NB cell viability, colony formation, migration, and invasion, and promoted cell cycle arrest and apoptosis in vitro, as well as decreased tumor growth in vivo. Mechanistically, DLX6‐AS1 operated as a miR‐513c‐5p sponge. MiR‐513c‐5p mediated the regulation of DLX6‐AS1 on NB cell malignant progression in vitro. PLK4 was a target of miR‐513c‐5p‐ and DLX6‐AS1‐controlled PLK4 expression via sponging miR‐513c‐5p. Furthermore, the suppressive effect of miR‐513c‐5p overexpression on NB cell malignant progression in vitro was reversed by PLK4 upregulation. Our findings identified a novel regulatory mechanism, the DLX6‐AS1/miR‐513c‐5p/PLK4 axis, in NB progression, highlighting a strong rationale for developing DLX6‐AS1 as a new target for NB management.