Evidence map›Paper›PMID 39273015›Full record

ArticleCells2024

Unraveling the Role of Bromodomain and Extra-Terminal Proteins in Human Uterine Leiomyosarcoma.

Qiwei Yang, Ali Falahati, Azad Khosh, Ricardo R Lastra, Thomas G Boyer, Ayman Al-Hendy

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cells, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. 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

6 authors.

Qiwei YangDepartment of Obstetrics and Gynecology, University of Chicago, Chicago, IL 60637, USA.ORCID 0000-0001-7131-8946
Ali FalahatiPoundbury Cancer Institute for Personalised Medicine, Dorchester DT1 3BJ, UK.
Azad KhoshDepartment of Molecular Medicine, Institute of Biotechnology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.ORCID 0000-0003-3267-4280
Ricardo R LastraDepartment of Pathology, University of Chicago, Chicago, IL 60637, USA.
Thomas G BoyerDepartment of Molecular Medicine, Institute of Biotechnology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Ayman Al-HendyDepartment of Obstetrics and Gynecology, University of Chicago, Chicago, IL 60637, USA.ORCID 0000-0002-8778-4447

Funding

Molecular basis of MED12 in the pathogenesis of uterine fibroidsR01HD087417 · NICHD · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI THOMAS G BOYER · 2017 to 2026
$3.4M
Pathological reprogramming of the m6A epitranscriptome in uterine fibroidsR01HD106285 · NICHD · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI AL-HENDY, AYMAN, BOYER, THOMAS G · 2021 to 2025
$3.2M
NICHD NIH HHS R01 HD087417NICHD NIH HHS R01 HD106285NIH HHS R01 HD106285
6 · The paper itself

Abstract

Uterine leiomyosarcoma (uLMS) is the most common type of uterine sarcoma, associated with poor prognosis, high rates of recurrence, and metastasis. Currently, the molecular mechanism of the origin and development of uLMS is limited. Bromodomain and extra-terminal (BET) proteins are involved in both physiological and pathological events. However, the role of BET proteins in the pathogenesis of uLMS is unknown. Here, we show for the first time that BET protein family members, BRD2, BRD3, and BRD4, are aberrantly overexpressed in uLMS tissues compared to the myometrium, with a significant change by histochemical scoring assessment. Furthermore, inhibiting BET proteins with their small, potent inhibitors (JQ1 and I-BET 762) significantly inhibited the uLMS proliferation dose-dependently via cell cycle arrest. Notably, RNA-sequencing analysis revealed that the inhibition of BET proteins with JQ1 and I-BET 762 altered several critical pathways, including the hedgehog pathway, EMT, and transcription factor-driven pathways in uLMS. In addition, the targeted inhibition of BET proteins altered several other epigenetic regulators, including DNA methylases, histone modification, and m

Indexed as

LeiomyosarcomaTranscription FactorsUterine NeoplasmsAzepinesBenzodiazepinesBromodomain Containing ProteinsCell Cycle CheckpointsCell Cycle ProteinsCell Line, TumorCell ProliferationEpigenesis, GeneticFemaleGene Expression Regulation, NeoplasticHumansMiddle AgedProteinsAzepinesBenzodiazepinesbromodomain and extra-terminal domain protein, humanBromodomain Containing ProteinsCell Cycle Proteins(+)-JQ1 compoundmolibresibProteinsTranscription FactorsTriazolesbromodomain and extra-terminal proteinEMTepigenomehedgehog pathwayI-BET 762JQ1m6A regulatorstranscriptional factorstranscriptome analysisuterine leiomyosarcoma

Identifiers

PMID39273015
PMCPMC11394028

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.