RETRACTED: Long non-coding RNA DLX6-AS1 regulates neuroblastoma progression by targeting YAP1 via miR-497-5p (Retracted article. See vol. 294, 2022)

被引:18
|
作者
Li, Changchun [1 ]
Wang, Shan [1 ]
Yang, Chao [1 ]
机构
[1] Chongqing Med Univ, Dept Pediat Surg Oncol,Chongqing Key Lab Pediat, Childrens Hosp,Minist Educ,China Int Sci & Techno, Key Lab Child Dev & Disorders,Natl Clin Res Ctr C, Chongqing, Peoples R China
关键词
Long non-coding RNA; DLX6-AS1; Neuroblastoma; miR-497-5p; YAP1; PROLIFERATION; BIOGENESIS; CANCER; CELLS;
D O I
10.1016/j.lfs.2020.117657
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Aims: The lncRNA distal-less homeobox 6 antisense 1 (DLX6-AS1) has been reported to be an oncogenic lncRNA in diverse malignant cancers; however, whether it has oncogenic role in neuroblastoma(NB) remain largely unknown. This study explored the expression status, function and potential mechanism of DLX6-AS1 in NB. Main method: In the current study, a total of 70 human NB tissues and matched adjacent non-tumor tissues were collected. Quantitative PCR (qPCR) was performed to study the expression differences of DLX6-AS1 in tissues and NB cell lines. Proliferation, migration, invasion and EMT status of transfected NB cells were evaluated by WST-1 assay, colony formation unit assay, Transwell assay and qPCR, respectively. The interaction between DLX6-AS1 and its potential targets was confirmed by luciferase reporter assay. Xenograft models were established to evaluate tumor proliferation in vivo. Key finding: We found that the expression of DLX6-AS1 was significantly increased in both NB tissues and cell lines, and elevated DLX6AS1 expression was positively correlated with advanced stage and poor survival. Proliferation rate, migration and invasion ability, as well as EMT process of NB cells was inhibited after DLX6AS1 knockdown, meanwhile, the tumor growth in vivo was impaired after DLX6-AS1 inhibition. Further analysis showed that DLX6-AS1 regulates the expression of YAP1 by sponging miR-497-5p. DLX6-AS1 directly interacts with miR-497-5p and reduces the binding of miR-497-5p to YAP1 3'UTR, thus inhibiting the degradation of YAP1 by miR-497-5p. Significance: This work demonstrates that DLX6-AS1 partially enhances the proliferation, migration and invasion abilities of NB cells through the miR-497-5p/YAP1 pathway, DLX6-AS1 might act as a promising therapeutic target for NB.
引用
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页数:9
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