ArticleOncotarget2018
miR-665 targets c-MYC and HDAC8 to inhibit murine neuroblastoma cell growth.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Review
- Article
- Article
- Long non-coding RNA NHEG1/hsa-miR-665/HMGB1 axis is involved in the regulation of neuroblastoma progression.Bioengineered · 2021Article
- RHPN1-AS1 promotes cell proliferation and migration via miR-665/Akt3 in ovarian cancer.Cancer gene therapy · 2021Article
- Olmesartan alleviates bleomycin-mediated vascular smooth muscle cell senescence via the miR-665/SDC1 axis.American journal of translational research · 2020Article
- Plasma MicroRNA Expression Profiles in Psoriasis.Journal of immunology research · 2020Article
- Identification of potential core genes and miRNAs in testicular seminoma via bioinformatics analysis.Molecular medicine reports · 2019Article
- miR-665 expression predicts poor survival and promotes tumor metastasis by targeting NR4A3 in breast cancer.Cell death & disease · 2019Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroblastoma is a common tumor of the peripheral nervous system in children. Highly aggressive MYC-driven neuroblastoma is defined by increased c-MYC and/or MYCN expression. This study employed a mouse neuroblastoma cell model to assess the role of miR-665 in tumorigenesis. We found that miR-665 suppresses mRNAs, targeting c-MYC and HDAC8, which are involved in neuroblastoma tumorigenesis. N6,2'-O-dibutyryladenosine 3':5'cyclic monophosphate (Bt2cAMP) inhibited neuroblastoma cell growth by inhibiting c-MYC and HDAC8 expression and activating caspase 3. Bt2cAMP also upregulated miR-665, and miR665 transfection mimicked the effects of Bt2cAMP, including reduced c-MYC and HDAC8 expression, increased caspase 3 activation, and reduced neuroblastoma cell growth. As compared to untreated cells, Bt2cAMP increased the number of cells in G1 phase by 50% and the number in G2-M phase by 5%, while the number of cells in S phase was reduced 2.8-fold. Similarly, miR-665 transfection increased the number of cells in G1 phase by 16% and the number in G2M phase by 2%, and decreased the cells in S-phase by 18%. These findings indicate miR-665 suppresses neuroblastoma tumorigenesis by inhibiting c-MYC and HDAC8 expression and suggest miR-665 has potential as an anti-neuroblastoma therapeutic.
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Registered trials
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