ArticleReproductive biology and endocrinology : RB&E2025
The role of long non-coding ribonucleic acid HOXA11-AS in endometriosis therapy.
Article in Reproductive biology and endocrinology : RB&E, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- Review
- HAGLR promotes endometriosis progression via the miR-185-5p/VEGFA axis and serves as a potential diagnostic biomarker.BMC women's health · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
objectiveTo investigate the function of HOXA11-antisense long non-coding RNA (HOXA11-AS) in endometriosis treatment response.
methodsTissue samples (ectopic and eutopic endometrium) were obtained from surgically diagnosed subjects with endometriosis (n = 15) and controls (n = 11) without endometriosis after treatment with a progestin. RNA was extracted from these tissues; cDNA was prepared and lncRNA HOXA11-AS levels were measured by quantitative real-time polymerase chain reaction (RT-qPCR). Immortalized endometrial stromal cells from an endometriosis patient (ENDO cell line) were cultured and transfected by HOXA11-AS plasmid and potential target genes were analyzed by RT-qPCR.
resultsProgestin therapy led to lower lncRNA HOXA11-AS expression. HOXA11-AS was most decreased in ectopic endometriotic lesions, lower by 81% compared to eutopic endometrium from women with endometriosis. There was no difference in progestin response between eutopic endometrium in endometriosis and normal endometrium from controls. A HOXA11-AS plasmid was used to increase HOXA11-AS expression in an endometriotic cell line. Increased HOXA11-AS led to a significant increase in the expression of genes ITGB3, AKT1, MMP2, and MMP9, which have a role in cell proliferation and tumorigenesis. HOXA11-AS also upregulated the mRNA levels of tumor suppressor and apoptotic regulatory genes PTEN, BCL2 and Caspase3.
conclusionsHOXA11-AS is a critical regulator of normal endometrial development. HOXA11-AS is elevated in endometriosis contributes to its pathophysiology. This long non-coding RNA was decreased in women undergoing endometriosis treatment with progestins. HOXA11-AS regulated several key drivers of disease and repression during treatment likely has a central role in preventing growth and invasion of endometriosis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.