Evidence map›Paper›PMID 16330772›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

MicroRNAs 221 and 222 inhibit normal erythropoiesis and erythroleukemic cell growth via kit receptor down-modulation.

Nadia Felli, Laura Fontana, Elvira Pelosi, Rosanna Botta, Desirée Bonci, Francesco Facchiano, Francesca Liuzzi, Valentina Lulli, Ornella Morsilli, Simona Santoro and 6 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 346 papers.

0numbers the graph read from it
0cells of the map it votes in
346citing papers in PubMed
19.5field-weighted citation impact, top 1% 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

346 citing papers in PubMed, 762 citations in OpenAlex.

  1. Review
  2. Current issues in molecular biology · 2026
    Article
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  8. MicroRNA Profiling in Chronic Limb-Threatening Ischemia Their Role in Arteriogenesis.The International journal of angiology : official publication of the International College of Angiology, Inc · 2025
    Article
  9. Review
  10. Article
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  12. Article
  13. Review
  14. Article
  15. Potential Use of MicroRNA Technology in Thalassemia Therapy.Journal of clinical medicine research · 2024
    Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Article

286 more citing papers are in PubMed but not listed here.

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

16 authors at 3 institutions in 2 countries.

Nadia FelliDepartment of Hematology, Oncology, and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy.
Laura Fontana
Elvira Pelosi
Rosanna Botta
Desirée Bonci
Francesco Facchiano
Francesca Liuzzi
Valentina Lulli
Ornella Morsilli
Simona Santoro
Mauro Valtieri
George Adrian Calin
Chang-Gong Liu
Antonio Sorrentino
Carlo M Croce
Cesare Peschle
Sidney Kimmel Cancer Center · USIstituto Superiore di Sanità · ITThomas Jefferson University · US

Funding

KDR--A NOVEL FUNCTIONAL HEMATOPOIETIC STEM CELL MARKERR01HL063168 · NHLBI · THOMAS JEFFERSON UNIVERSITY · PI PESCHLE, CESARE · 2001 to 2004
$1.2M
NHLBI NIH HHS 1R01 HL63168NHLBI NIH HHS R01 HL063168
6 · The paper itself

Abstract

MicroRNAs (miRs) are small noncoding RNAs that regulate gene expression primarily through translational repression. In erythropoietic (E) culture of cord blood CD34+ progenitor cells, the level of miR 221 and 222 is gradually and sharply down-modulated. Hypothetically, this decline could promote erythropoiesis by unblocking expression of key functional proteins. Indeed, (i) bioinformatic analysis suggested that miR 221 and 222 target the 3' UTR of kit mRNA; (ii) the luciferase assay confirmed that both miRs directly interact with the kit mRNA target site; and (iii) in E culture undergoing exponential cell growth, miR down-modulation is inversely related to increasing kit protein expression, whereas the kit mRNA level is relatively stable. Functional studies show that treatment of CD34+ progenitors with miR 221 and 222, via oligonucleotide transfection or lentiviral vector infection, causes impaired proliferation and accelerated differentiation of E cells, coupled with down-modulation of kit protein: this phenomenon, observed in E culture releasing endogenous kit ligand, is magnified in E culture supplemented with kit ligand. Furthermore, transplantation experiments in NOD-SCID mice reveal that miR 221 and 222 treatment of CD34+ cells impairs their engraftment capacity and stem cell activity. Finally, miR 221 and 222 gene transfer impairs proliferation of the kit+ TF-1 erythroleukemic cell line. Altogether, our studies indicate that the decline of miR 221 and 222 during exponential E growth unblocks kit protein production at mRNA level, thus leading to expansion of early erythroblasts. Furthermore, the results on kit+ erythroleukemic cells suggest a potential role of these miRs in cancer therapy.

Indexed as

AnimalsAntigens, CD34Cell DifferentiationCell ProliferationComputational BiologyErythropoiesisFetal BloodGene Expression ProfilingGene Expression RegulationHematopoietic Stem CellsHumansLuciferasesMiceMice, Inbred NODMice, SCIDMicroRNAsAntigens, CD34LuciferasesMicroRNAsProto-Oncogene Proteins c-kit

Identifiers

PMID16330772
PMCPMC1312381
OpenAlexW2087206434

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.