Evidence map›Paper›PMID 39737119›Full record

ArticleCytoJournal2024

Inhibition of lysine-specific histone demethylase 1A suppresses adenomyosis through reduction in ectopic endometrial stromal cell proliferation, migration, and invasion.

Limei Cui, Changmei Sang, Ruoqing Li, Shuping Zhao

Abstract read
In one paragraph

Article in CytoJournal, 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. Review
  4. Article
  5. Signaling pathways and advances in targeted therapy for adenomyosis.Frontiers in cell and developmental biology · 2025
    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

4 authors.

Limei CuiDepartment of Gynecology , Qingdao Women and Children's Hospital, Shandong University, Qingdao, China.
Changmei SangDepartment of Gynecology, Qingdao Women and Children's Hospital, Qingdao, China.
Ruoqing LiMedical College, Qingdao University, Qingdao, Shandong, China.
Shuping ZhaoDepartment of Gynecology , Qingdao Women and Children's Hospital, Shandong University, Qingdao, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Deep endometriosis is now referred to as adenomyosis externa, whereas adenomyosis is once known as endometriosis interna. Lysine-specific histone demethylase 1A (KDM1A, commonly LSD1) is a lysine demethylase that targets histone and non-histone proteins. This study aimed to assess how KDM1A affects the migration, invasion, and proliferation of adenomyosis-derived endometrial stromal cells (ESCs). Material and Methods: Immunocytochemistry staining was used to identify primary ectopic endometrial stromal cells (EESCs) and eutopic endometrial stromal cells (EuESCs) were isolated and purified from patients with complete hysterectomy for adenomyosis. Cell counting kit-8 assay, colony formation, wound scratch, and transwell assays were used to investigate the effect of silencing KDM1A on the inhibition cell viability, colony, migration, and invasion, respectively. Mechanistic investigations were carried out by Western blot and quantitative real-time polymerase chain reaction (qRT-PCR). Results: Vimentin staining was highly positive and cytokeratin staining was nearly negative in EESCs and EuESCs. KDM1A silencing reduced the ability of EESCs and EuESCs to proliferate ( Conclusion: In adenomyosis, silencing KDM1A can limit the motility, invasiveness, and proliferation of EuESCs and EESCs. These outcomes could potentially correlate with the decreased expression levels of matrix metalloproteinases (MMP)-2, MMP-9, Fascin, and Erzin proteins.

Indexed as

adenomyosisendometrial stromal cellslysine-specific histone demethylase 1Ametastasis migrationproliferation

Identifiers

PMID39737119
PMCPMC11683409

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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.