Evidence map›Paper›PMID 20124487›Full record

ArticleCancer research2010

Transcription factor KLF11 integrates progesterone receptor signaling and proliferation in uterine leiomyoma cells.

Ping Yin, Zhihong Lin, Scott Reierstad, Ju Wu, Hiroshi Ishikawa, Erica E Marsh, Joy Innes, Youhong Cheng, Kerry Pearson, John Sayler Coon and 3 more

Open access · greenAbstract read
In one paragraph

Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

41 citing papers in PubMed, 88 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Review
  4. UTERINE FIBROIDS.Physiological reviews · 2025
    Review
  5. Review
  6. ACSL4-mediated H3K9 and H3K27 hyperacetylation upregulates SNAIL to drive TNBC metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Cardiometabolic Risk Factors and Benign Gynecologic Disorders.Obstetrical & gynecological survey · 2019
    Review
  16. Article
  17. Article
  18. A Role for Progesterone-Regulated sFRP4 Expression in Uterine Leiomyomas.The Journal of clinical endocrinology and metabolism · 2017
    Article
  19. Article
  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

13 authors at 1 institution in 1 country.

Ping YinDivision of Reproductive Biology Research, Department of Obstetrics and Gynecology, Feinberg School of Medicine at Northwestern University, Chicago, IL 60611, USA.
Zhihong Lin
Scott Reierstad
Ju Wu
Hiroshi Ishikawa
Erica E Marsh
Joy Innes
Youhong Cheng
Kerry Pearson
John Sayler Coon
J Julie Kim
Debabrata Chakravarti
Serdar E Bulun
Northwestern University · US

Funding

MULTIDISCIPLINARY CLINICAL AND TRANSLATIONAL SCIENCE (MCTS) PROGRAM (UL1)UL1RR025741 · NCRR · NORTHWESTERN UNIVERSITY AT CHICAGO · PI GREENLAND, PHILIP · 2008 to 2011
$24.7M
Uterine Leiomyoma Research Center ProgramP01HD057877 · NICHD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI CHAKRAVARTI, DEBABRATA · 2009 to 2019
$12.2M
ESTROGEN BIOSYNTHESIS AND UTERINE LEIOMYOMATAR01HD046260 · NICHD · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BULUN, SERDAR E · 2003 to 2007
$1.2M
NCRR NIH HHS UL1 RR025741NICHD NIH HHS P01 HD057877NICHD NIH HHS P01HD057877NICHD NIH HHS R01 HD046260
6 · The paper itself

Abstract

Uterine leiomyoma is the most common tumor of the female genital tract and the leading cause of hysterectomy. Although progesterone stimulates the proliferation of uterine leiomyoma cells, the mechanism of progesterone action is not well understood. We used chromatin immunoprecipitation (ChIP)-cloning approach to identify progesterone receptor (PR) target genes in primary uterine leiomyoma smooth muscle cells. We identified 18 novel PR-binding sites, one of which was located 20.5 kb upstream of the transcriptional start site of the Krüppel-like transcription factor 11 (KLF11) gene. KLF11 mRNA levels were minimally downregulated by progesterone but robustly upregulated by the progesterone antagonist RU486. Luciferase reporter assays showed significant baseline and RU486-inducible promoter activity in the KLF11 basal promoter or distal PR-binding region, both of which contained multiple Sp1-binding sequences but lacked classic progesterone response elements. RU486 stimulated recruitment of Sp1, RNA polymerase II, PR, and the coactivators SRC-1 and SRC-2 to the distal region and basal promoter. siRNA knockdown of PR increased KLF11 expression, whereas knockdown of KLF11 increased leiomyoma cell proliferation and abolished the antiproliferative effect of RU486. In vivo, KLF11 expression was significantly lower in leiomyoma tissues compared with adjacent myometrial tissues. Taken together, using a ChIP-cloning approach, we uncovered KLF11 as an integrator of PR signaling and proliferation in uterine leiomyoma cells.

Indexed as

Cell ProliferationApoptosis Regulatory ProteinsCell Cycle ProteinsFemaleGene Expression Regulation, NeoplasticHormone AntagonistsHumansLeiomyomaMifepristoneProgesteronePromoter Regions, GeneticReceptors, ProgesteroneRepressor ProteinsSignal TransductionTrans-ActivatorsTranscription FactorsApoptosis Regulatory ProteinsCell Cycle ProteinsHormone AntagonistsKLF11 protein, humanMifepristoneProgesteroneReceptors, ProgesteroneRepressor ProteinsTrans-ActivatorsTranscription Factors

Identifiers

PMID20124487
PMCPMC2822899
OpenAlexW2116591759

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.