Evidence map›Paper›PMID 22492871›Full record

ArticleThe Journal of clinical endocrinology and metabolism2012

Endometrial miR-181a and miR-98 expression is altered during transition from normal into cancerous state and target PGR, PGRMC1, CYP19A1, DDX3X, and TIMP3.

Harekrushna Panda, Tsai-Der Chuang, Xiaoping Luo, Nasser Chegini

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2012. 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
2.8field-weighted citation impact, top 10% 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, 75 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Harekrushna PandaDepartment of Obstetrics and Gynecology, University of Florida, Gainesville, Florida 32610, USA.
Tsai-Der Chuang
Xiaoping Luo
Nasser Chegini
University of Florida · US

Funding

MOLECULAR MECHANISM OF LEIOMYOMA GROWTH AND REGRESSIONR01HD037432 · NICHD · UNIVERSITY OF FLORIDA · PI SCHULTZ, GREGORY SCOTT · 2001 to 2011
$2.7M
Expression, hormonal regulation and function of microRNA in leiomyomaR01HD058664 · NICHD · UNIVERSITY OF FLORIDA · PI SCHULTZ, GREGORY SCOTT · 2009 to 2012
$1.4M
NICHD NIH HHS HD37432NICHD NIH HHS HD58664NICHD NIH HHS R01 HD037432NICHD NIH HHS R01 HD058664
6 · The paper itself

Abstract

contextEvidence suggests that a number of microRNA (miRNA) are aberrantly expressed in endometrial disorders with potential posttranscriptional regulation of their specific target genes, including ovarian steroid receptors.

objectivesOur objective was to assess the endometrial expression of miR-98 and miR-181a and their respective target genes, progesterone (P4) receptor membrane component 1 (PGRMC1) and P4 receptor (PGR). DESIGN, SETTING, AND PATIENTS: We evaluated tissue expression and in vitro regulation at an academic university medical center in endometrial biopsies and endometrial tissues from follicular and luteal phases with and without exposure to hormonal therapies and grade I-III endometrial cancer (n = 52).

interventionsINTERVENTIONS included endometrial biopsies and in vitro transfection.

main outcome measuresWe evaluated expression and function of miR-98 and miR-181a.

resultsAberrant expression of miR-98 and miR-181a is associated with endometrial transition from normal into cancerous states, which to some extent is influenced by hormonal milieu, and exhibited an inverse relationship with PGMRC1 and PGR expression, respectively. Treatments of Ishikawa cells with 17β-estradiol, P4, or medroxyprogesterone acetate had limited effects on miR-98, miR-181a, and PGRMC1 expression, whereas 17β-estradiol treatment increased PGR expression. In Ishikawa cells, gain of function of miR-98 repressed PGRMC1 and CYP19A1, and miR-181a repressed PGR, DDX3X, and TIMP3 at mRNA and protein levels through direct interactions with their respective 3'-untranslated regions and CCNE1 through miR-181a-induced DDX3X repression, with miR-98 reducing the rate of cell proliferation as compared with controls.

conclusionmiR-98 and miR-181a through their regulatory functions on PGRMC1, PGR, CYP19A1, TIMP3, and DDX3X expression may influence a wide range of endometrial cellular activities during normal menstrual cycle and transition into disease states, including endometrial cancer.

Indexed as

AdultAgedAromataseCarcinoma, EndometrioidCell Transformation, NeoplasticDEAD-box RNA HelicasesEndometrial NeoplasmsEndometriumFemaleGene Expression Regulation, NeoplasticHumansMembrane ProteinsMicroRNAsMiddle AgedPrecancerous ConditionsReceptors, ProgesteroneAromataseCYP19A1 protein, humanDDX3X protein, humanDEAD-box RNA HelicasesMembrane ProteinsMicroRNAsMIrn181 microRNA, humanMIRN98 microRNA, humanPGRMC1 protein, humanReceptors, ProgesteroneTIMP3 protein, humanTissue Inhibitor of Metalloproteinase-3

Identifiers

PMID22492871
PMCPMC3387391
OpenAlexW1994505064

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.