4.7 Article Retracted Publication

被撤回的出版物: Risk-Associated Long Noncoding RNA FOXD3-AS1 Inhibits Neuroblastoma Progression by Repressing PARP1-Mediated Activation of CTCF (Retracted article. See vol. 31, pg. 1857, 2023)

期刊

MOLECULAR THERAPY
卷 26, 期 3, 页码 755-773

出版社

CELL PRESS
DOI: 10.1016/j.ymthe.2017.12.017

关键词

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资金

  1. National Natural Science Foundation of China [81272779, 81372667, 81472363, 81402301, 81402408, 81572423, 81672500, 81773094, 81772967]
  2. Fundamental Research Funds for the Central Universities [2012QN224, 2013ZHYX003, 01-18-530112, 01-18-530115]
  3. Natural Science Foundation of Hubei Province [2014CFA012]

向作者/读者索取更多资源

Neuroblastoma (NB) is the most common extracranial tumor in childhood. Recent studies have implicated the emerging roles of long noncoding RNAs (lncRNAs) in tumorigenesis and aggressiveness. However, the functions and targets of risk-associated lncRNAs in NB progression still remain to be determined. Herein, through mining of public microarray datasets, we identify IncRNA forkhead box D3 antisense RNA 1 (FOXD3-AS1) as an independent prognostic marker for favorable outcome of NB patients. FOXD3-AS1 is downregulated in NB tissues and cell lines, and ectopic expression of FOXD3-AS1 induces neuronal differentiation and decreases the aggressiveness of NB cells in vitro and in vivo. Mechanistically, as a nuclear lncRNA, FOXD3-AS1 interacts with poly(ADP-ribose) polymerase 1 (PARP1) to inhibit the poly(ADP-ribosyl)ation and activation of CCCTC-binding factor (CTCF), resulting in derepressed expression of downstream tumor-suppressive genes. Rescue experiments indicate that FOXD3-AS1 harbors tumor-suppressive properties by inhibiting the oncogenic roles of PARP1 or CTCF and plays crucial roles in all-trans-retinoic-acid-mediated therapeutic effects on NB. Administration of FOXD3-AS1 construct or siRNAs against PARP1 or CTCF reduces the tumor growth and prolongs the survival of nude mice. These findings suggest that as a risk-associated lncRNA, FOXD3-AS1 inhibits the progression of NB through repressing PARP1-mediated CTCF activation.

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