MiR‐204, down‐regulated in retinoblastoma, regulates proliferation and invasion of human retinoblastoma cells by targeting CyclinD2 and MMP‐9

Xian-jin, WU; Zeng, Yong; Wu, Songbin; Zhong, Jixin; Wang, YuZhou; Xu, Junfa

doi:10.1016/j.febslet.2015.01.030

Cited by 65 publications

(46 citation statements)

References 30 publications

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“…The study has shown that NEAT1 aggravated the lipopolysaccharide (LPS)‐induced rat mesangial cell injury by modulating miR‐204 expression (Y. Chen, Qiu, et al, ). And miR‐204 has been found to be downregulated in RB tissues and cells, and it could suppress the proliferation and invasion of human RB cells (Wu et al, ). Consistent with previous data, we also found miR‐204 expression was decreased in RB tissues and cells (Figure b,c).…”

Section: Resultsmentioning

confidence: 99%

Long noncoding RNA NEAT1 promotes the growth of human retinoblastoma cells via regulation of miR‐204/CXCR4 axis

Zhong

Yang

et al. 2018

Journal Cellular Physiology

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Retinoblastoma (RB) is an aggressive eye cancer of infancy and childhood with high mortality. Studies have shown that long noncoding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) is closely related to the progression of multiple cancers. However, its role in RB remains unknown. This study aimed to investigate the role and underlying mechanism of NEAT1 in RB. We first detected the expression of NEAT1 in human RB tissues and cell lines. The effects of NEAT1 on the proliferation, migration, and apoptosis of RB cells were analyzed by loss‐of‐function. The underlying mechanism of NEAT1 in RB was mainly focused on the microRNA 204/C‐X‐C chemokine receptor type 4 (miR‐204/CXCR4) axis. In addition, the role and mechanism of NEAT1 in RB were further evaluated in a mouse xenograft tumor model. We found NEAT1 and CXCR4 expression levels were elevated, whereas miR‐204 expression was decreased in RB tissues and cells. Downregulation of NEAT1 significantly decreased the proliferation and migration but promoted the apoptosis of RB cells. NEAT1 functioned as a competing endogenous RNA for miR‐204 to regulate CXCR4 expression. Knockdown of NEAT1 suppressed the tumor volume, tumor weight, and CXCR4 expression, whereas increased miR‐204 expression in mice. In conclusion, NEAT1 promotes the development of RB via miR‐204/CXCR4 axis, which provides a new target for the treatment of RB disease.

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Section: Resultsmentioning

confidence: 99%

Long noncoding RNA NEAT1 promotes the growth of human retinoblastoma cells via regulation of miR‐204/CXCR4 axis

Zhong

Yang

et al. 2018

Journal Cellular Physiology

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“…The miR-204 is a well-characterized microRNA, already shown to be downregulated in many solid tumors [15, 18, 19]. Despite the fact that its mode of action and its effector targets may differ according to the tissue of origin and the stage of the tumor, there is indication that it may represent a general tumor suppressor [15, 18–24]. Thus, the data collected here for both GC and CC specimens and the experiments performed in the GTL-16 and HUCCT1 cells are in line with the literature data.…”

Section: Discussionmentioning

confidence: 99%

MiR-204 down-regulation elicited perturbation of a gene target signature common to human cholangiocarcinoma and gastric cancer

Canu¹,

Sacconi²,

Lorenzon³

et al. 2017

Oncotarget

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Background & AimsThere is high need of novel diagnostic and prognostic tools for tumors of the digestive system, such as gastric cancer and cholangiocarcinoma. We recently found that miR-204 was deeply downregulated in gastric cancer tissues. Here we investigated whether this was common to other tumors of the digestive system and whether this elicited a miR-204-dependent gene target signature, diagnostically and therapeutically relevant. Finally, we assessed the contribution of the identified target genes to the cell cycle progression and clonogenicity of gastric cancer and cholangiocarcinoma cell lines.MethodsWe employed quantitative PCR and Affymetrix profiling for gene expression studies. In silico analysis aided us to identifying a miR-204 target signature in publicly available databases (TGCA). We employed transient transfection experiments, clonogenic assays and cell cycle profiling to evaluate the biological consequences of miR-204 perturbation.ResultsWe identified a novel miR-204 gene target signature perturbed in gastric cancer and in cholangiocarcinoma specimens. We validated its prognostic relevance and mechanistically addressed its biological relevance in GC and CC cell lines.ConclusionsWe suggest that restoring the physiological levels of miR-204 in some gastrointestinal cancers might be exploited therapeutically.

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“…Downregulation of miR-204 (~2.5-fold) has been observed in human retinoblastoma (RB) tissues and cell lines when compared to normal pediatric retinas [182]. Restoration of miR-204 levels inhibited RB cell migration and invasion capability in vitro and decreased RB tumor growth in vivo.…”

Section: Mir-204 In Glaucoma and Retinoblastomamentioning

confidence: 99%

TRPM3_miR-204: a complex locus for eye development and disease

Shiels

2020

Hum Genomics

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First discovered in a light-sensitive retinal mutant of Drosophila, the transient receptor potential (TRP) superfamily of non-selective cation channels serve as polymodal cellular sensors that participate in diverse physiological processes across the animal kingdom including the perception of light, temperature, pressure, and pain. TRPM3 belongs to the melastatin sub-family of TRP channels and has been shown to function as a spontaneous calcium channel, with permeability to other cations influenced by alternative splicing and/or non-canonical channel activity. Activators of TRPM3 channels include the neurosteroid pregnenolone sulfate, calmodulin, phosphoinositides, and heat, whereas inhibitors include certain drugs, plant-derived metabolites, and G-protein subunits. Activation of TRPM3 channels at the cell membrane elicits a signal transduction cascade of mitogen-activated kinases and stimulus response transcription factors. The mammalian TRPM3 gene hosts a non-coding microRNA gene specifying miR-204 that serves as both a tumor suppressor and a negative regulator of post-transcriptional gene expression during eye development in vertebrates. Ocular co-expression of TRPM3 and miR-204 is upregulated by the paired box 6 transcription factor (PAX6) and mutations in all three corresponding genes underlie inherited forms of eye disease in humans including early-onset cataract, retinal dystrophy, and coloboma. This review outlines the genomic and functional complexity of the TRPM3_miR-204 locus in mammalian eye development and disease.

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MiR‐204, down‐regulated in retinoblastoma, regulates proliferation and invasion of human retinoblastoma cells by targeting CyclinD2 and MMP‐9

Cited by 65 publications

References 30 publications

Long noncoding RNA NEAT1 promotes the growth of human retinoblastoma cells via regulation of miR‐204/CXCR4 axis

Long noncoding RNA NEAT1 promotes the growth of human retinoblastoma cells via regulation of miR‐204/CXCR4 axis

MiR-204 down-regulation elicited perturbation of a gene target signature common to human cholangiocarcinoma and gastric cancer

TRPM3_miR-204: a complex locus for eye development and disease

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