Long noncoding RNA DLX6-AS1 promotes neuroblastoma progression by regulating miR-107/BDNF pathway

Zhang, Huan-Yu; Xing, Maoqing; Guo, Jing; Zhao, Jinchuan; Chen, Xin; Jiang, Zhong; Zhang, Hong; Dong, Qi

doi:10.1186/s12935-019-0968-x

Cited by 30 publications

(31 citation statements)

References 25 publications

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“…[20][21][22] Recent studies reported that DLX6-AS1 was overexpressed in NB and promoted NB malignant progression by functioning as an available miRNA sponge. 4,12 The results reported here provide a novel molecular explanation for the oncogenic role of DLX6-AS1 in NB.…”

Section: Discussionmentioning

confidence: 72%

“…Recent reports showed that DLX6-AS1 functioned as a tumor promoter in NB. 4,12 To validate the crucial effect of DLX6-AS1 on NB progression, we first examined the level of DLX6-AS1 in NB tissues and cells using qRT-PCR. The data showed that DLX6-AS1 expression was prominently upregulated in NB tissues compared to the matched normal tissues (Figure 1a).…”

Section: Dlx6-as1 Level Was Significantly Increased In Nb Tissues Amentioning

confidence: 99%

“…Lei et al uncovered that DLX6‐AS1 sequestered miR‐124‐3p to promote the development of pediatric Ewing's sarcoma 11 . Moreover, previous studies reported that DLX6‐AS1, a significantly overexpressed lncRNA in NB, enhanced NB malignant progression 4,12 . Although the two reports also demonstrated the function of DLX6‐AS1 as a miRNA sponge, our understanding of its molecular basis in NB progression is still limited.…”

Section: Introductionmentioning

confidence: 99%

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Silencing of long non‐coding RNADLX6‐AS1 weakens neuroblastoma progression by the miR‐513c‐5p/PLK4 axis

et al. 2020

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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.

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Section: Discussionmentioning

confidence: 72%

Section: Dlx6-as1 Level Was Significantly Increased In Nb Tissues Amentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Silencing of long non‐coding RNADLX6‐AS1 weakens neuroblastoma progression by the miR‐513c‐5p/PLK4 axis

et al. 2020

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“…Inhibition of lncRNA XIST reduces the NBL tumor volume in mice 38 . Long noncoding RNA DLX6‐AS1 silencing impedes NBL tumor growth 39 . Similarly, LINC01410 knockdown alleviated the tumor growth in mice, indicating the important function of silencing LINC01410 in suppressing NBL tumorigenesis in vivo.…”

Section: Discussionmentioning

confidence: 95%

Long noncoding RNA LINC01410 promotes the tumorigenesis of neuroblastoma cells by sponging microRNA‐506‐3p and modulating WEE1

Han

Zhang

et al. 2020

Cancer Medicine

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Objective Neuroblastoma (NBL) is an extra‐cranial solid tumor in children. This study was attempted to investigate the regulatory mechanism of long noncoding RNA LINC01410 (LINC01410) on NBL. Methods The expression of LINC01410, miR‐506‐3p, and WEE1 in NBL was evaluated by quantitative real time polymerase chain reaction. The proliferation and colony formation ability of NBL cells were analyzed by MTT and colony formation assay. Flow cytometry assay was executed to measure the apoptosis and cell cycle. Dual‐luciferase reporter assay was used to detect the targeted relationships among LINC01410, miR‐506‐3p, and WEE1. Additionally, the role of LINC01410 on NBL in vivo was evaluated according to a tumor xenograft model. Results The expression of LINC01410 and WEE1 was enhanced and miR‐506‐3p was inhibited in NBL. LINC01410 knockdown attenuated the cell proliferation, colony formation ability, and inhibited tumor growth. Moreover, LINC01410 silencing facilitated the apoptosis and arrested the cell cycle. LINC01410 interacted with miR‐506‐3p to elevate the WEE1 expression in NBL. Additionally, miR‐506‐3p inhibition or WEE1 overexpression weakened the reduction effects of sh‐LINC01410 on cell proliferation, colony formation ability, apoptosis, and cell cycle. Conclusions Knockdown of LINC01410 inhibited the development of NBL by miR‐506‐3p/WEE1 axis in vitro, which could serve as a potential therapeutic target for NBL therapy.

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“…Limited studies introduced that DLX6-AS1 was abundantly expressed in NB tissues and cell lines, and DLX6-AS1 downregulation-impaired cell proliferation, metastasis and invasion in NB cells. 27 Besides, high expression of DLX6-AS1 was associated with advanced stage and poor survival. 28 Here, consistent with these previous studies, the aberrant overexpression of DLX6-AS1 was observed in NB tissues and cells.…”

Section: Discussionmentioning

confidence: 99%

<p>LncRNA DLX6-AS1 Promotes the Progression of Neuroblastoma by Activating STAT2 via Targeting miR-506-3p</p>

Hu¹,

Sun²,

Hu³

et al. 2020

CMAR

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Background: Neuroblastoma (NB) is a common malignant tumor of the sympathetic nervous system, mainly disturbing children. Long non-coding RNAs (lncRNAs) serving as promising cancer biomarkers have been well recognized. Our study intends to explore the functions of lncRNA X-inactive specific transcript (DLX6-AS1) in NB and provide a potential action mechanism. Methods: The expression of DLX6-AS1, miR-506-3p and signal transducer and activator of transcription 2 (STAT2) was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation was assessed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and colony formation assay. Cell cycle distribution was determined by flow cytometry assay. The protein level of cell cycle-related markers and STAT2 was detected by Western blot. Glycolysis progress was evaluated according to glucose consumption, lactate production and ATP level. The target genes were predicted by the online database Starbase3.0 and verified by dual-luciferase reporter assay. Results: DLX6-AS1 expression was highly elevated in NB tissues and cells. DLX6-AS1 deficiency inhibited NB cell proliferation, cell cycle and glycolysis in vitro. MiR-506-3p was a target of DLX6-AS1, and miR-506-3p absence partly reversed the effects of DLX6-AS1 deficiency. Besides, STAT2 was targeted by miR-506-3p, and its expression was regulated by DLX6-AS1 through miR-506-3p. MiR-506-3p restoration also inhibited NB cell malignant behaviors, and STAT2 overexpression partially abolished the role of miR-506-3p restoration. Moreover, DLX6-AS1 deficiency weakened tumor growth in vivo. Conclusion: DLX6-AS1 regulated cell proliferation, cell cycle and glycolysis in vitro and tumor growth in vivo to promote the development of NB by upregulating STAT2 via targeting miR-506-3p.

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Long noncoding RNA DLX6-AS1 promotes neuroblastoma progression by regulating miR-107/BDNF pathway

Cited by 30 publications

References 25 publications

Silencing of long non‐coding RNADLX6‐AS1 weakens neuroblastoma progression by the miR‐513c‐5p/PLK4 axis

Silencing of long non‐coding RNADLX6‐AS1 weakens neuroblastoma progression by the miR‐513c‐5p/PLK4 axis

Long noncoding RNA LINC01410 promotes the tumorigenesis of neuroblastoma cells by sponging microRNA‐506‐3p and modulating WEE1

<p>LncRNA DLX6-AS1 Promotes the Progression of Neuroblastoma by Activating STAT2 via Targeting miR-506-3p</p>

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