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open-access journal published nature publishing group nature portfolio phu6-puro-nf90-shrna lentivirus particles privacy policy mir-590-5p-dependent post-transcriptional repression nature advertising bioinformatics tools ethanol solutions sheep anti-dig-horseradish peroxidase mir-590-5p-deleted cells grown sheep anti-dig-hrp conjugate putative mir-590-5p-binding site 0/ reprints mir-590-5p-deleted crc cells vegfa small-interfering rna mir-590-5p knockdown-induced angiogenesis data establish mir-590-5p enzyme-linked immunosorbent assay sw480-mir-590-5p inhibitor group ht29 mir-590-5p-deficient cells hrp-conjugated secondary antibody microrna-15b-5p shuttled mir-590-5p significantly reduced nf45/nf90 heterodimer contributes anti-rabbit secondary antibody rna-induced silencing complex dna-binding complex regulating squamous cell carcinoma 6 μm-thick paraffin sections strong pro-metastasis phenotype author correspondence mir-590-5p sponge inhibitor hrp substrate 3-amino-9-ethylcarbazole radio-immunoprecipitation assay buffer sw620-mir-590-5p groups 100 nm psicheck-2-nf90 3′utr mir-590-5p target sequence colorectal cancer inhibits synthetic mir-590-5p mimic cold serum-free medium 200 μl serum-free medium increases mature mir-590-5p sw620-mir-590-5p group compared sw620-mir-590-5p clones inhibiting nf90/vegfa axis pgem-t-easy vector brain-enriched mir-7 biogenesis wild-type hct116 cells

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      headline:MiR-590-5p inhibits colorectal cancer angiogenesis and metastasis by regulating nuclear factor 90/vascular endothelial growth factor A axis
      description:Altered expression of microRNA-590-5p (miR-590-5p) is involved in tumorigenesis, however, its role in colorectal cancer (CRC) remains to be determined. In this study, we focused on examining the effects of different expression levels of miR-590-5p in cancer cells and normal cells. Results showed that there are lower expression levels of miR-590-5p in human CRC cells and tissues than in normal control cells and tissues. Similarly, in our xenograft mouse model, knockdown of miR-590-5p promoted the progression of CRC. However, an overexpression of miR-590-5p in the mice inhibited angiogenesis, tumor growth, and lung metastasis. Nuclear factor 90 (NF90), a positive regulator of vascular endothelial growth factor (VEGF) mRNA stability and protein synthesis, was shown to be a direct target of miR-590-5p. The overexpression of NF90 restored VEGFA expression and rescued the loss of tumor angiogenesis caused by miR-590-5p. Conversely, the NF90-shRNA attenuated the increased tumor progression caused by the miR-590-5p inhibitor. Clinically, the levels of miR-590-5p were inversely correlated with those of NF90 and VEGFA in CRC tissues. Furthermore, knockdown of NF90 lead to a reduction of pri-miR-590 and an increase of mature miR-590-5p, suggesting a negative feedback loop between miR-590-5p and NF90. Collectively, these data establish miR-590-5p as an anti-onco-miR that inhibits CRC angiogenesis and metastasis through a new mechanism involving NF90/VEGFA signaling axis, highlighting the potential of miR-590-5p as a target for human CRC therapy.
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