Evidence map›Paper›PMID 27602152›Full record

ArticleOncology letters2016

Action of HMGB1 on miR-221/222 cluster in neuroblastoma cell lines.

Emanuela Mari, Alessandra Zicari, Flavia Fico, Isabella Massimi, Lolli Martina, Stefania Mardente

Abstract read
In one paragraph

Article in Oncology letters, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed.

  1. Article
  2. Article
  3. CD34Cells · 2022
    Article
  4. Article
  5. Insulin Resistance and Cancer: In Search for a Causal Link.International journal of molecular sciences · 2021
    Review
  6. Review
  7. Signaling Modulation byFrontiers in cell and developmental biology · 2021
    Article
  8. Review
  9. Article
  10. Article
  11. Oncotarget · 2018
    Article
  12. Article
  13. Article
  14. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Emanuela MariDepartment of Experimental Medicine, Sapienza University of Rome, I-00161 Rome, Italy.
Alessandra ZicariDepartment of Experimental Medicine, Sapienza University of Rome, I-00161 Rome, Italy.
Flavia FicoDepartment of Experimental Medicine, Sapienza University of Rome, I-00161 Rome, Italy.
Isabella MassimiDepartment of Experimental Medicine, Sapienza University of Rome, I-00161 Rome, Italy.
Lolli MartinaDepartment of Experimental Medicine, Sapienza University of Rome, I-00161 Rome, Italy.
Stefania MardenteDepartment of Experimental Medicine, Sapienza University of Rome, I-00161 Rome, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

microRNA (miR/miRNA) are small non-coding RNAs that control gene expression at the post-transcriptional level by targeting mRNAs. Aberrant expression of miRNAs is often observed in different types of cancer. Specific miRNAs function as tumor suppressors or oncogenes and interfere with various aspects of carcinogenesis, including differentiation, proliferation and invasion. Upregulation of miRNAs 221 and 222 has been shown to induce a malignant phenotype in numerous human cancers via inhibition of phosphatase and tensin homolog (PTEN) expression. Neuroblastoma is the most common extracranial solid malignancy in children, which is characterized by cellular heterogeneity that corresponds to different clinical outcomes. The different cellular phenotypes are associated with different gene mutations and miRs that control genetic and epigenetic factors. For this reason miRs are considered a potential therapeutic target in neuroblastoma. The aim of the present study was to investigate the mechanisms by which extracellular high mobility group box 1 (HMGB1) promotes cell growth in neuroblastoma. SK-N-BE(2) and SH-SY5Y neuroblastoma derived cell lines were transfected with the antisense oligonucleotides, anti-miR-221 and -222, followed by treatment with HMGB1 to investigate the expression of the oncosuppressor PTEN. In this study, it was demonstrated that HMGB1, which is released by damaged cells and tumor cells, upregulates miR-221/222 oncogenic clusters in the two human neuroblastoma derived cell lines. The results revealed that the oncogenic cluster miRs 221/222 were more highly expressed by the most undifferentiated cell line [SK-N-BE(2)] compared with the the less tumorigenic cell line (SH-SY5Y) and that exogenous HMGB1 increases this expression. In addition, HMGB1 modulates PTEN expression via miR-221/222, as demonstrated by transiently blocking miR-221/222 with anti-sense oligonucleotides. These results may lead to the development of novel therapeutic strategies for neuroblastoma.

Indexed as

AKT signalingcluster miR-221/222high mobility group box 1MYCNneuroblastomaphosphatase and tensin homolog

Identifiers

PMID27602152
PMCPMC4998517

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.