Evidence map›Paper›PMID 21454583›Full record

ArticleThe Journal of biological chemistry2011

miRNA-205 suppresses melanoma cell proliferation and induces senescence via regulation of E2F1 protein.

Altaf A Dar, Shahana Majid, David de Semir, Mehdi Nosrati, Vladimir Bezrookove, Mohammed Kashani-Sabet

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 3 pooled it
9.2field-weighted citation impact, top 2% 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

124 citing papers in PubMed, 3 syntheses or guidelines pooled it, 258 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Trial
  6. Article
  7. Article
  8. Article
  9. Review
  10. The E2F family: a ray of dawn in cardiomyopathy.Molecular and cellular biochemistry · 2025
    Review
  11. Non-Coding RNAs in Breast Cancer: Diagnostic and Therapeutic Implications.International journal of molecular sciences · 2024
    Review
  12. Article
  13. Review
  14. A New Approach to Melanoma Treatment: microRNAs.Current topics in medicinal chemistry · 2024
    Review
  15. Review
  16. Review
  17. Article
  18. microRNA-205 in prostate cancer: Overview to clinical translation.Biochimica et biophysica acta. Reviews on cancer · 2022
    Review
  19. Article
  20. Article

64 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

6 authors at 2 institutions in 1 country.

Altaf A DarCalifornia Pacific Medical Center Research Institute, San Francisco, California 94107, USA.
Shahana Majid
David de Semir
Mehdi Nosrati
Vladimir Bezrookove
Mohammed Kashani-Sabet
California Pacific Medical Center · USUniversity of California, San Francisco · US

Funding

Validation of Genomic Targets in MelanomaR01CA114337 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KASHANI-SABET, MOHAMMED · 2005 to 2015
$3.2M
Molecular Classification of Primary Cutaneous MelanomaR01CA122947 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KASHANI-SABET, MOHAMMED · 2007 to 2011
$1.5M
NCI NIH HHS CA114337NCI NIH HHS CA122947NCI NIH HHS R01 CA114337NCI NIH HHS R01 CA122947
6 · The paper itself

Abstract

MicroRNAs (miRNAs) regulate gene expression by repressing translation or directing sequence-specific degradation of complementary mRNA. Here, we report that expression of miR-205 is significantly suppressed in melanoma specimens when compared with nevi and is correlated inversely with melanoma progression. miRNA target databases predicted E2F1 and E2F5 as putative targets. The expression levels of E2F1 and E2F5 were correlated inversely with that of miR-205 in melanoma cell lines. miR-205 significantly suppressed the luciferase activity of reporter plasmids containing the 3'-UTR sequences complementary to either E2F1 or E2F5. Overexpression of miR-205 in melanoma cells reduced E2F1 and E2F5 protein levels. The proliferative capacity of melanoma cells was suppressed by miR-205 and mediated by E2F-regulated AKT phosphorylation. miR-205 overexpression resulted in induction of apoptosis, as evidenced by increased cleaved caspase-3, poly-(ADP-ribose) polymerase, and cytochrome c release. Stable overexpression of miR-205 suppressed melanoma cell proliferation, colony formation, and tumor cell growth in vivo and induced a senescence phenotype accompanied by elevated expression of p16INK4A and other markers for senescence. E2F1 overexpression in miR-205-expressing cells partially reversed the effects on melanoma cell growth and senescence. These results demonstrate a novel role for miR-205 as a tumor suppressor in melanoma.

Indexed as

Gene Expression Regulation, Neoplastic3' Untranslated RegionsApoptosisCell Line, TumorCell ProliferationCell SurvivalCellular SenescenceE2F1 Transcription FactorE2F5 Transcription FactorHumansMelanomaMicroRNAsModels, BiologicalPoly(ADP-ribose) PolymerasesSkin Neoplasms3' Untranslated RegionsE2F1 Transcription FactorE2F5 protein, humanE2F5 Transcription FactorMicroRNAsMIR205, humanPoly(ADP-ribose) Polymerases

Identifiers

PMID21454583
PMCPMC3089503
OpenAlexW2036672958

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.