MiR‐181a/b induce the growth, invasion, and metastasis of neuroblastoma cells through targeting ABI1

Liu, Xiaodan; Peng, Hongxia; Luo, A-Li; Cai, Mansi; He, Jing; Zhang, Xiaohong; Luo, Ziyan; Jiang, Hua; Xu, Ling

doi:10.1002/mc.22839

Cited by 31 publications

(17 citation statements)

References 59 publications

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“…Dysregulation of certain miRNAs has been implicated in the pathogenesis of NB [7]. For example, miR-181a/b is significantly upregulated in aggressive neuroblastoma, which enhanced its tumorigenesis and progression by suppressing the expression of ABI1 [8]. Our previous studies show that miR-145 inhibits the NB progression through targeting hypoxia-inducible factor 2 alpha (HIF-2α) [9].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2019

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BackgroundLong noncoding RNAs (lncRNAs) play essential roles in tumor progression. However, the functions and targets of lncRNAs in neuroblastoma (NB) progression still remain to be determined. In this study, we aimed to investigate the effect of lncRNA DLX6 antisense RNA 1 (DLX6-AS1) on NB and the underlying mechanism involved.MethodsThrough mining of public microarray datasets, we identify aberrantly expressed lncRNAs in NB. The gene expression levels were determined by quantitative real-time PCR, and protein expression levels were determined by western blot assay. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, colony formation assay, wound-healing assay, transwell invasion assays and flow cytometry analysis were utilized to examine cell proliferation, migration, invasion and apoptosis. Luciferase reporter assay was performed to confirm the interaction between DLX6-AS1and its potential targets. Tumor xenograft assay was used to verify the role of DLX6-AS1 in NB in vivo.ResultsWe identified DLX6-AS1 was upregulated in NB by using a public microarray dataset. The expression of DLX6-AS1 was increased in NB tissues and derived cell lines, and high expression of DLX6-AS1 was positively correlated with advanced TNM stage and poor differentiation. Knockdown of DLX6-AS1 induced neuronal differentiation, apoptosis and inhibited the growth, invasion, and metastasis of NB cells in vitro and impaired tumor growth in vivo. MiR-107 was the downstream target of DLX6-AS1. MiR-107 was found to target brain‐derived neurotrophic factor (BDNF) which is an oncogene in NB. Knockdown of miR-107 or overexpression of BDNF reversed the suppression of NB progression caused by DLX6-AS1 silence.ConclusionOverall, our finding supports that DLX6-AS1 promotes NB progression by regulating miR-107/BDNF pathway, acting as a novel therapeutic target for NB.

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Section: Introductionmentioning

confidence: 99%

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

et al. 2019

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“…Particularly, this pertains to the top candidate, humanspecific ZNF702P at 19q13.4. As ENCORI database mining reveals, ZNF702P RNA binds NB metastasis-associated miR-181a-5p and miR-23a-3p (Cheng et al, 2014;Gibert et al, 2014;Liu et al, 2018). Thus, ZNF702P can be responsible for the up-regulation of miR-181a targets in kalirin-GEF1-inhibited cells.…”

Section: Discussionmentioning

confidence: 99%

Kalirin-RAC controls nucleokinetic migration in ADRN-type neuroblastoma

et al. 2021

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The migrational propensity of neuroblastoma is affected by cell identity, but the mechanisms behind the divergence remain unknown. Using RNAi and time-lapse imaging, we show that ADRN-type NB cells exhibit RAC1- and kalirin-dependent nucleokinetic (NUC) migration that relies on several integral components of neuronal migration. Inhibition of NUC migration by RAC1 and kalirin-GEF1 inhibitors occurs without hampering cell proliferation and ADRN identity. Using three clinically relevant expression dichotomies, we reveal that most of up-regulated mRNAs in RAC1- and kalirin–GEF1–suppressed ADRN-type NB cells are associated with low-risk characteristics. The computational analysis shows that, in a context of overall gene set poverty, the upregulomes in RAC1- and kalirin–GEF1–suppressed ADRN-type cells are a batch of AU-rich element–containing mRNAs, which suggests a link between NUC migration and mRNA stability. Gene set enrichment analysis–based search for vulnerabilities reveals prospective weak points in RAC1- and kalirin–GEF1–suppressed ADRN-type NB cells, including activities of H3K27- and DNA methyltransferases. Altogether, these data support the introduction of NUC inhibitors into cancer treatment research.

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“…The increased expression of the examined four genes gain more importance in the context of their extensive gene network. Zhx2 (also known as RAF ) has previously been associated with Hodgkin lymphoma [65] and hepatocellular carcinoma [66]; Abi1 (abl interactor 1) has a role in colorectal carcinoma development and invasion [67] and also in neuroblastoma propagation [68]. Aberrant function of Tcf4 (transcription factor 4) has been reported in glioblastoma [69] and in colorectal tumors [70].…”

Section: Discussionmentioning

confidence: 99%

Tyrosine Kinase Inhibitor Imatinib Mesylate Alters DMBA-Induced Early Onco/Suppressor Gene Expression with Tissue-Specificity in Mice

Gergely

Murnyák

Bencze

et al. 2019

BioMed Research International

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Tyrosine kinases play crucial roles in cellular development and tumorigenesis. Tyrosine kinase inhibitors (TKIs) are effective and widely used drug molecules in targeted cancer therapies. Altered expressions of protooncogenes and tumor suppressor genes after DMBA (7,12-dimethylbenz[a]anthracene) treatment have been described as early markers of tumor induction; however their tissue-specific effects remain still unclear. Our study was aimed at examining the short-term possible antineoplastic and chemopreventive effects of a TKI compound (imatinib mesylate) on a DMBA-induced mouse tumor model. In addition, we also investigated the tissue-specific expressions of Hras, Kras, Myc, and Trp53 genes in the brain, bone marrow, spleen, liver, abdominal lymph nodes, thymus, lungs, and kidneys, respectively. 24 hours after the imatinib mesylate injection, we observed significant Kras downregulation in the bone marrow and lung of the DMBA-treated mice. Moreover, the mRNA expression of Myc was also found to be decreased significantly in the spleen. Interestingly, while Trp53 expression was significantly increased in the lung, it was decreased in the other tissues. However, there was also a tendency in the decreased Myc level in the bone marrow, brain, kidneys, lungs, and lymph nodes and in the decreased Hras level in the bone marrow, kidneys, and lungs, although no significant differences were observed. Our findings indicate rapid tissue-specific impact of imatinib mesylate on DMBA-induced gene expression in vivo, supporting the chemopreventive potential of imatinib mesylate in cancer.

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MiR‐181a/b induce the growth, invasion, and metastasis of neuroblastoma cells through targeting ABI1

Cited by 31 publications

References 59 publications

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

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

Kalirin-RAC controls nucleokinetic migration in ADRN-type neuroblastoma

Tyrosine Kinase Inhibitor Imatinib Mesylate Alters DMBA-Induced Early Onco/Suppressor Gene Expression with Tissue-Specificity in Mice

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