Evidence map›Paper›PMID 21643017›Full record

ArticleOncogene2012

MiR-100 regulates cell differentiation and survival by targeting RBSP3, a phosphatase-like tumor suppressor in acute myeloid leukemia.

Y-S Zheng, H Zhang, X-J Zhang, D-D Feng, X-Q Luo, C-W Zeng, K-Y Lin, H Zhou, L-H Qu, P Zhang and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 4% 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

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Remics: a redescription-based framework for multi-omics analysis.Frontiers in cell and developmental biology · 2026
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  7. Review
  8. Unveiling the hemolymphatic miRNome composition of the schistosomiasis vector snailCurrent research in parasitology & vector-borne diseases · 2025
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Benzene Exposure and MicroRNAs Expression: In Vitro, In Vivo and Human Findings.International journal of environmental research and public health · 2023
    Review
  14. BioMed research international · 2023
    Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

16 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

11 authors at 3 institutions in 1 country.

Y-S ZhengKey Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory for Biocontrol, Sun Yat-sen University, Guangzhou, China.
H Zhang
X-J Zhang
D-D Feng
X-Q Luo
C-W Zeng
K-Y Lin
H Zhou
L-H Qu
P Zhang
Y-Q Chen
Sun Yat-sen University · CNArmy Medical University · CNThe First Affiliated Hospital, Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute myeloblastic leukemia (AML) is characterized by the accumulation of abnormal myeloblasts (mainly granulocyte or monocyte precursors) in the bone marrow and blood. Though great progress has been made for improvement in clinical treatment during the past decades, only minority with AML achieve long-term survival. Therefore, further understanding mechanisms of leukemogenesis and exploring novel therapeutic strategies are still crucial for improving disease outcome. MicroRNA-100 (miR-100), a small non-coding RNA molecule, has been reported as a frequent event aberrantly expressed in patients with AML; however, the molecular basis for this phenotype and the statuses of its downstream targets have not yet been elucidated. In the present study, we found that the expression level of miR-100 in vivo was related to the stage of the maturation block underlying the subtypes of myeloid leukemia. In vitro experiments further demonstrated that miR-100 was required to promote the cell proliferation of promyelocytic blasts and arrest them differentiated to granulocyte/monocyte lineages. Significantly, we identified RBSP3, a phosphatase-like tumor suppressor, as a bona fide target of miR-100 and validated that RBSP3 was involved in cell differentiation and survival in AML. Moreover, we revealed a new pathway that miR-100 regulates G1/S transition and S-phase entry and blocks the terminal differentiation by targeting RBSP3, which partly in turn modulates the cell cycle effectors pRB/E2F1 in AML. These events promoted cell proliferation and blocked granulocyte/monocyte differentiation. Our data highlight an important role of miR-100 in the molecular etiology of AML, and implicate the potential application of miR-100 in cancer therapy.

Indexed as

Cell DifferentiationCell Line, TumorCell SurvivalE2F1 Transcription FactorFemaleHumansLeukemia, Myeloid, AcuteMaleMicroRNAsPhosphorylationRetinoblastoma ProteinTumor Suppressor ProteinsCTDSPL protein, humanE2F1 protein, humanE2F1 Transcription FactorMicroRNAsMIRN100 microRNA, humanRetinoblastoma ProteinTumor Suppressor Proteins

Identifiers

PMID21643017
PMCPMC3253429
OpenAlexW2028251862

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.