miR-331-3p regulates expression of neuropilin-2 in glioblastoma

Epis, Michael R.; Giles, Keith M.; Candy, Patrick A.; Webster, Rebecca; Leedman, Peter J.

doi:10.1007/s11060-013-1271-7

Cited by 57 publications

(53 citation statements)

References 38 publications

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“…Therefore, we hypothesized that the miR‐331‐3p and syndecan‐1 axis may contribute to prostate cancer progression. MiR‐331‐3p exerts significant cell growth retardation in gastric cancer and glioblastoma , whereas it drives metastasis and is associated with clinically poor prognosis in hepatocellular carcinoma . In the present study, cell proliferation was suppressed in miR‐331‐3p precursor‐transfected PC3 cells, whereas miR‐331‐3p induced EMT.…”

Section: Discussionsupporting

confidence: 46%

Syndecan-1 up-regulates microRNA-331-3p and mediates epithelial-to-mesenchymal transition in prostate cancer

et al. 2015

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MicroRNAs (miRNAs) are small noncoding RNAs with a length of approximately 19-24 nucleotides that regulate gene expression through translational inhibition and contribute to the progression of various tumors including prostate cancer. Aberrant expression of miRNAs has been implicated in the progression and metastasis of prostate cancer. The present study aimed to investigate whether miR-331-3p controlled by syndecan-1 positively affects the epithelial-to-mesenchymal transition (EMT). Overexpression of miR-331-3p upregulated mesenchymal markers such as vimentin, N-cadherin, and snail and downregulated epithelial markers such as E-cadherin and desmoplakin in the prostate cancer cell line PC3. We identified Neuropilin 2 and nucleus accumbens-associated protein 1 as putative target molecules in silico, as they were closely associated with the expression of miR-331-3p and TGF-β/Smad 4 signals. In situ hybridization and immunohistochemistry of radical prostatectomy samples revealed miR-331-3p in cancer cells with high Gleason patterns, in which EMT was demonstrated by decreased E-cadherin, and increased vimentin staining. Syndecan-1 gene silencing decreased levels of Dicer, which is involved in miRNA maturation. MiR-331-3p-mediated miRNA maturation and enhanced EMT via effects on TGF-β/Smad 4 and Dicer are essential for the development of prostate cancer mediated by syndecan-1. © 2015 Wiley Periodicals, Inc.

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Section: Discussionsupporting

confidence: 46%

Syndecan-1 up-regulates microRNA-331-3p and mediates epithelial-to-mesenchymal transition in prostate cancer

et al. 2015

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“…Although NRP2 gene amplification appears to be common in ESCC, it is unlikely that this represents the sole mechanism leading to NRP2 up‐regulation, since we found a number of clinical samples that did not have chromosome 2p amplified, but had NRP2 overexpressed. Studies of glioblastoma and pancreatic cancer have identified other potential mechanisms of NRP2 up‐regulation, including miR‐331‐3p and interleukin‐8 deregulation .…”

Section: Discussionmentioning

confidence: 99%

Neuropilin-2 promotes tumourigenicity and metastasis in oesophageal squamous cell carcinoma through ERK-MAPK-ETV4-MMP-E-cadherin deregulation

Fung

Tong

et al. 2016

J. Pathol.

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Oesophageal squamous cell carcinoma (ESCC) is the most common histological subtype of oesophageal cancer. The disease is particularly prevalent in southern China. The incidence of the disease is on the rise and its overall survival rate remains dismal. Identification and characterization of better molecular markers for early detection and therapeutic targeting are urgently needed. Here, we report levels of transmembrane and soluble neuropilin-2 (NRP2) to be significantly up-regulated in ESCC, and to correlate positively with advanced tumour stage, lymph node metastasis, less favourable R category and worse overall patient survival. NRP2 up-regulation in ESCC was in part a result of gene amplification at chromosome 2q. NRP2 overexpression promoted clonogenicity, angiogenesis and metastasis in ESCC in vitro, while NRP2 silencing by lentiviral knockdown or neutralizing antibody resulted in a contrary effect. This observation was extended in vivo in animal models of subcutaneous tumourigenicity and tail vein metastasis. Mechanistically, overexpression of NRP2 induced expression of ERK MAP kinase and the transcription factor ETV4, leading to enhanced MMP-2 and MMP-9 activity and, as a consequence, suppression of E-cadherin. In summary, NRP2 promotes tumourigenesis and metastasis in ESCC through deregulation of ERK-MAPK-ETV4-MMP-E-cadherin signalling. NRP2 represents a potential diagnostic or prognostic biomarker and therapeutic target for ESCC. Copyright © 2016 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

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“…Nrp1-targeting strategies have shown promise in preclinical models and might serve as adjuvants to VEGF-targeting antiangiogenic agents [39]. Nrp2 binds VEGFC and D to promote lymphangiogenesis, which facilitates tumor progression [38, 40]. Thus, therapeutic strategies that are able to block both Nrp1 and 2 could offer enhanced clinical benefit by inhibiting both angiogenesis and lymphangiogenesis.…”

Section: Hs In Tumor Angiogenesismentioning

confidence: 99%

Heparan sulfate signaling in cancer

Knelson

Nee

Blobe

2014

Trends in Biochemical Sciences

160

168

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Summary Heparan sulfate (HS) is a biopolymer consisting of variably sulfated repeating disaccharide units. The anticoagulant heparin is a highly sulfated intracellular variant of HS. HS has demonstrated roles in embryonic development, homeostasis, and human disease via non-covalent interactions with numerous cellular proteins, including growth factors and their receptors. HS can function as a co-receptor by enhancing receptor-complex formation. In other contexts, HS disrupts signaling complexes or serves as a ligand sink. The effects of HS on growth factor signaling are tightly regulated by the actions of sulfyltransferases, sulfatases and heparanases. HS has important emerging roles in oncogenesis and heparin derivatives represent potential therapeutic strategies for human cancers. Here we review recent insights into HS signaling in tumor proliferation, angiogenesis, metastasis, and differentiation. A cancer-specific understanding of HS signaling could uncover potential therapeutic targets in this highly actionable signaling network.

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miR-331-3p regulates expression of neuropilin-2 in glioblastoma

Cited by 57 publications

References 38 publications

Syndecan-1 up-regulates microRNA-331-3p and mediates epithelial-to-mesenchymal transition in prostate cancer

Syndecan-1 up-regulates microRNA-331-3p and mediates epithelial-to-mesenchymal transition in prostate cancer

Neuropilin-2 promotes tumourigenicity and metastasis in oesophageal squamous cell carcinoma through ERK-MAPK-ETV4-MMP-E-cadherin deregulation

Heparan sulfate signaling in cancer

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