Evidence map›Paper›PMID 33951281›Full record

ReviewWiley interdisciplinary reviews. RNA2021

The many facets of miR-223 in cancer: Oncosuppressor, oncogenic driver, therapeutic target, and biomarker of response.

Andrea Favero, Ilenia Segatto, Tiziana Perin, Barbara Belletti

Open access · greenAbstract readReview
In one paragraph

Review in Wiley interdisciplinary reviews. RNA, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% of its field
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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. The potential role of miR-155 in the tumorigenesis of cervical cancer.Frontiers in cell and developmental biology · 2025
    Review
  10. Article
  11. Article
  12. Review
  13. MCPIP1 modulates the miRNA‒mRNA landscape in keratinocyte carcinomas.Journal of experimental & clinical cancer research : CR · 2024
    Article
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
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  20. Review
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

4 authors at 1 institution in 1 country.

Andrea FaveroMolecular Oncology Unit, Centro di Riferimento Oncologico di Aviano (CRO Aviano), IRCCS, National Cancer Institute, Aviano, Italy.ORCID 0000-0002-6053-8182
Ilenia SegattoMolecular Oncology Unit, Centro di Riferimento Oncologico di Aviano (CRO Aviano), IRCCS, National Cancer Institute, Aviano, Italy.ORCID 0000-0001-5282-1028
Tiziana PerinPathology Unit, Centro di Riferimento Oncologico di Aviano (CRO Aviano), IRCCS, National Cancer Institute, Aviano, Italy.ORCID 0000-0002-9823-0167
Barbara BellettiMolecular Oncology Unit, Centro di Riferimento Oncologico di Aviano (CRO Aviano), IRCCS, National Cancer Institute, Aviano, Italy.ORCID 0000-0003-2249-0285
Centro di Riferimento Oncologico · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Given their intrinsic pleiotropism, microRNAs (miR) play complex biological roles, in both normal and pathological conditions. Often the same miR can act as oncogene or oncosuppressor, depending on the biological process dysregulated in each specific tissue. miR-223 does not represent an exception to this rule and its functions greatly differ in different contexts. miR-223 has been widely studied in the hematopoietic compartment, where it plays a central role in innate immune response, regulating myeloid differentiation and granulocytes function. Accordingly, dysregulated expression of miR-223 has been associated to different inflammatory disorders and tumors arising from the immune compartment. Most carcinomas, breast cancer being the most studied, display loss of miR-223. However, in gastro-esophageal cancers miR-223 is frequently overexpressed and correlates with worse prognosis. A link between miR-223 and response to CDK4/6-inhibitors has been recently proposed, suggesting a role as biomarker of therapeutic response. The notion that one of the most commonly mutated protein in cancer, mutant p53, binds the promoter of miR-223 and suppresses its transcription, adds a further level of complexity to the full understanding of miR-223 in cancer. In this review, we will summarize the current knowledge on the molecular networks that alter or are altered by miR-223, in different cancer types. We will discuss if the times are ready for the exploitation of miR-223 as predictive biomarker of treatment response or, even, as therapeutic target, in specific settings. Finally, we will suggest which could be the next steps to be taken for a realistic clinical application of miR-223. This article is categorized under: RNA in Disease and Development > RNA in Disease.

Indexed as

MicroRNAsNeoplasmsBiomarkersCarcinogenesisGene Expression Regulation, NeoplasticHumansOncogenesBiomarkersMicroRNAsMIR223, humanbiomarkerbreast cancercancermicroRNAmiR-223

Identifiers

PMID33951281
PMCPMC8518860
OpenAlexW3158209645

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.