A Proteomics Approach to Investigate miR-153-3p and miR-205-5p Targets in Neuroblastoma Cells

Patil, Ketan S.; Basak, Indranil; Pal, Ramavati; Ho, Hsin-Pin; Alves, Guido; Chang, Emmanuel J.; Larsen, Jan Petter; Møller, Simon Geir

doi:10.1371/journal.pone.0143969

Cited by 24 publications

(17 citation statements)

References 56 publications

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“…Alpha‐synuclein aggregation was recently identified as essential to apoptotic neurons in PD . It was also observed to be downregulated by miR‐153‐3p and miR‐205‐5p in neuroblastoma cells, suggesting its potential as a tumor suppressor . In the present study, the anti‐apoptotic function and invasion ability of MB cells, rather than cell proliferation, were increased after SNCA siRNA transfection, but decreased after overexpression of the gene, indicating the potential tumor suppressor function of SNCA in MB.…”

Section: Discussionsupporting

confidence: 57%

SNCA, a novel biomarker for Group 4 medulloblastomas, can inhibit tumor invasion and induce apoptosis

Jiang

et al. 2018

Cancer Science

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Medulloblastoma (MB) is the most common malignant brain tumor in childhood. It contains at least four distinct molecular subgroups. The aim of this study is to explore novel diagnostic and potential therapeutic markers within each subgroup of MB, in particular within Group 4, the largest subgroup, to facilitate diagnosis together with gene therapy. One hundred and six MB samples were examined. Tumor subtype was evaluated with the NanoString assay. Several novel tumor related genes were shown to have high subgroup sensitivity and specificity, including PDGFRA,FGFR1, and ALK in the WNT group, CCND1 in the SHH group, and α‐synuclein (SNCA) in Group 4. Knockdown and overexpression assays of SNCA revealed the ability of this gene to inhibit tumor invasion and induce apoptosis. Methylation‐specific PCR and pyrosequencing analysis showed that epigenetic mechanisms, rather than DNA hypermethylation, might play the key role in the regulation of SNCA expression in MB tumors. In conclusion, we identify SNCA as a novel diagnostic biomarker for Group 4 MB. Some other subgroup signature genes have also been found as candidate therapeutic targets for this tumor.

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Section: Discussionsupporting

confidence: 57%

SNCA, a novel biomarker for Group 4 medulloblastomas, can inhibit tumor invasion and induce apoptosis

Jiang

et al. 2018

Cancer Science

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“…[27][28][29] Recent reports point out that OS in RPE cells intensifies the production and release of angiogenic factors, thus increasing the formation of new blood vessels. 18,32,33 In agreement with this, miR-205-5p overexpression also reduced reactive oxygen species (ROS) by increasing peroxiredoxin 2 levels, 34 suggesting that miR-205-5p could be sensitive to oxidative stimuli. 18,32,33 In agreement with this, miR-205-5p overexpression also reduced reactive oxygen species (ROS) by increasing peroxiredoxin 2 levels, 34 suggesting that miR-205-5p could be sensitive to oxidative stimuli.…”

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confidence: 56%

Oxidative stress‐induced angiogenesis is mediated by miR‐205‐5p

Oltra

Vidal-Gil

Maisto³

et al. 2019

J Cellular Molecular Medi

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miR‐205‐5p is known to be involved in VEGF‐related angiogenesis and seems to regulate associated cell signalling pathways, such as cell migration, proliferation and apoptosis. Therefore, several studies have focused on the potential role of miR‐205‐5p as an anti‐angiogenic factor. Vascular proliferation is observed in diabetic retinopathy and the ‘wet’ form of age‐related macular degeneration. Today, the most common treatments against these eye‐related diseases are anti‐VEGF therapies. In addition, both AMD and DR are typically associated with oxidative stress; hence, the use of antioxidant agents is accepted as a co‐adjuvant therapy for these patients. According to previous data, ARPE‐19 cells release pro‐angiogenic factors when exposed to oxidative insult, leading to angiogenesis. Matching these data, results reported here, indicate that miR‐205‐5p is modulated by oxidative stress and regulates VEGFA‐angiogenesis. Hence, miR‐205‐5p is proposed as a candidate against eye‐related proliferative diseases.

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“…According to the study from Patil K et al miR-153-3p plays an important role in neuroprotection, which could down-regulate key proteins involved in Parkinson’s disease [ 29 ]. We thus speculated that miR-153-3p might be a tumor suppressor participating in the development of glioma.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-153-3p enhances cell radiosensitivity by targeting BCL2 in human glioma

Sun

Piao

2018

Biol Res

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BackgroundGlioma is the most prevalent malignant tumor in human central nervous systems. Recently, the development of resistance to radiotherapy in glioma patients markedly vitiates the therapy outcome. MiR-153-3p has been reported to be closely correlated with tumor progression, but its effect and molecular mechanism underlying radioresistance remains unclear in glioma.MethodsThe expression of miR-153-3p was determined in radioresistant glioma clinical specimens as well as glioma cell lines exposed to irradiation (IR) using quantitative real-time PCR. Cell viability, proliferation and apoptosis were then evaluated by MTT assay, colony formation assay, Flow cytometry analysis and caspase-3 activity assay in glioma cells (U87 and U251). Tumor forming was evaluated by nude mice model in vivo. TUNEL staining was used to detect cell apoptosis in nude mice model. The target genes of miR-153-3p were predicted and validated using integrated bioinformatics analysis and a luciferase reporter assay.ResultsHere, we found that miR-153-3p was down-regulated in radioresistant glioma clinical specimens as well as glioma cell lines (U87 and U251) exposed to IR. Enhanced expression of miR-153-3p promoted the radiosensitivity, promoted apoptosis and elevated caspase-3 activity in glioma cells in vitro, as well as the radiosensitivity in U251 cell mouse xenografs in vivo. Mechanically, B cell lymphoma-2 gene (BCL2) was identified as the direct and functional target of miR-153-3p. Moreover, restoration of BCL2 expression reversed miR-153-3p-induced increase of radiosensitivity, apoptosis and caspase-3 activity in U251 cells in vitro. In addition, clinical data indicated that the expression of miR-153-3p was significantly negatively associated with BCL2 in radioresistance of glioma samples.ConclusionsOur findings suggest that miR-153-3p is a potential target to enhance the effect of radiosensitivity on glioma cells, thus representing a new potential therapeutic target for glioma.

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A Proteomics Approach to Investigate miR-153-3p and miR-205-5p Targets in Neuroblastoma Cells

Cited by 24 publications

References 56 publications

SNCA, a novel biomarker for Group 4 medulloblastomas, can inhibit tumor invasion and induce apoptosis

SNCA, a novel biomarker for Group 4 medulloblastomas, can inhibit tumor invasion and induce apoptosis

Oxidative stress‐induced angiogenesis is mediated by miR‐205‐5p

MicroRNA-153-3p enhances cell radiosensitivity by targeting BCL2 in human glioma

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