Evidence map›Paper›PMID 24287487›Full record

ArticleNature communications2013

Cyclin D1 induction of Dicer governs microRNA processing and expression in breast cancer.

Zuoren Yu, Liping Wang, Chenguang Wang, Xiaoming Ju, Min Wang, Ke Chen, Emanuele Loro, Zhiping Li, Yuzhen Zhang, Kongming Wu and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

42 citing papers in PubMed, 74 citations in OpenAlex.

  1. Article
  2. Research and development prospects of TRIM65.Journal of cancer research and clinical oncology · 2025
    Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. The double dealing of cyclin D1.Cell cycle (Georgetown, Tex.) · 2020
    Review
  16. Article
  17. Article
  18. Article
  19. Cell cycle regulation and hematologic malignancies.Blood science (Baltimore, Md.) · 2019
    Review
  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

18 authors at 5 institutions in 2 countries.

Zuoren Yu1] Department of Cancer Biology, Thomas Jefferson University, 233 South 10th Street, Philadelphia, Pennsylvania 19107, USA [2] Kimmel Cancer Center, Thomas Jefferson University, 233 South 10th Street, Philadelphia, Pennsylvania 19107, USA [3] Research Center for Translational Medicine, Key Laboratory for Basic Research in Cardiology, East Hospital, Tongji University School of Medicine, 150 Jimo Road, Shanghai 200120, China.
Liping Wang
Chenguang Wang
Xiaoming Ju
Min Wang
Ke Chen
Emanuele Loro
Zhiping Li
Yuzhen Zhang
Kongming Wu
Mathew C Casimiro
Michael Gormley
Adam Ertel
Paolo Fortina
Yihan Chen
Aydin Tozeren
Zhongmin Liu
Richard G Pestell
Thomas Jefferson University · USShanghai East Hospital · CNSidney Kimmel Cancer Center · USDrexel University · USHuazhong University of Science and Technology · CN

Funding

X-Ray Crystallography and Macromolecular CharacterizationP30CA056036 · NCI · THOMAS JEFFERSON UNIVERSITY · PI CHRISTINE M. EISCHEN · 1995 to 2026
$94.8M
Initiation and Maintenance In Mammary TumorigenesisR01CA075503 · NCI · YESHIVA UNIVERSITY · PI PESTELL, RICHARD G · 1998 to 2011
$4.6M
CYCLIN D1 FUNCTION IN PROSTATE CANCERR01CA086072 · NCI · YESHIVA UNIVERSITY · PI PESTELL, RICHARD G · 2001 to 2013
$3.3M
REGULATION OF CYCLIN D1 EXPRESSIONR01CA070896 · NCI · YESHIVA UNIVERSITY · PI PESTELL, RICHARD G · 2000 to 2010
$3.2M
DACH1/Eya Cell fate determination factor and mammary tumorigenesisR01CA132115 · NCI · THOMAS JEFFERSON UNIVERSITY · PI PESTELL, RICHARD G · 2009 to 2018
$3.1M
Cyclin D1 Regulation of Nuclear Receptor Function in Breast CancerR01CA107382 · NCI · THOMAS JEFFERSON UNIVERSITY · PI PESTELL, RICHARD G · 2004 to 2008
$1.6M
NCI NIH HHS P30 CA056036NCI NIH HHS P30CA056036NCI NIH HHS R01 CA070896NCI NIH HHS R01CA070896NCI NIH HHS R01 CA075503NCI NIH HHS R01CA075503NCI NIH HHS R01 CA086072NCI NIH HHS R01CA086072NCI NIH HHS R01 CA107382NCI NIH HHS R01CA107382NCI NIH HHS R01 CA132115NCI NIH HHS R01CA132115
6 · The paper itself

Abstract

Cyclin D1 encodes the regulatory subunit of a holoenzyme that phosphorylates the pRB protein and promotes G1/S cell-cycle progression and oncogenesis. Dicer is a central regulator of miRNA maturation, encoding an enzyme that cleaves double-stranded RNA or stem-loop-stem RNA into 20-25 nucleotide long small RNA, governing sequence-specific gene silencing and heterochromatin methylation. The mechanism by which the cell cycle directly controls the non-coding genome is poorly understood. Here we show that cyclin D1(-/-) cells are defective in pre-miRNA processing which is restored by cyclin D1a rescue. Cyclin D1 induces Dicer expression in vitro and in vivo. Dicer is transcriptionally targeted by cyclin D1, via a cdk-independent mechanism. Cyclin D1 and Dicer expression significantly correlates in luminal A and basal-like subtypes of human breast cancer. Cyclin D1 and Dicer maintain heterochromatic histone modification (Tri-m-H3K9). Cyclin D1-mediated cellular proliferation and migration is Dicer-dependent. We conclude that cyclin D1 induction of Dicer coordinates microRNA biogenesis.

Indexed as

Gene Expression Regulation, NeoplasticAnimalsBreast NeoplasmsCell MovementCell ProliferationCyclin D1FemaleHCT116 CellsHistonesHumansMammary Neoplasms, ExperimentalMCF-7 CellsMiceMice, Inbred C57BLMice, TransgenicMicroRNAsCyclin D1HistonesMicroRNAsRibonuclease III

Identifiers

PMID24287487
PMCPMC3874416
OpenAlexW2056028275

What OpenQuestion holds

Textmetadata
LicenceTDM
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.