LncRNA HOTAIR regulates cell invasion and migration in endometriosis through miR-519b-3p/PRRG4 pathway
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⤵ 13 in-corpus citations
Abstract
Endometriosis is a common benign disease in gynecology and has malignant biological behaviors, such as hyperplasia, invasion, metastasis, and recurrence. However, the pathogenesis of endometriosis remains unclear. The present study aimed to investigate whether LncRNA HOTAIR regulates cell invasion and migration in endometriosis by regulating the miR-519b-3p/PRRG4 pathway. The qRT-PCR results showed that the average relative expression of LncRNA HOTAIR was much higher in ectopic endometrial tissues than in eutopic endometrial tissues. Scratch and transwell assays showed that the cell migration and invasion ability of LncRNA HOTAIR overexpression group was significantly higher than those in the control group. Conversely, the LncRNA HOTAIR knockdown group showed the opposite results. Bioinformatics analysis suggested that the downstream target genes of LncRNA HOTAIR were miR-519b-3p and Prrg4. Knockdown of LncRNA HOTAIR can reduce the up-regulation of Prrg4 by miR-519b-3p and then inhibit the invasion and migration ability of endometrial stromal cells. In Conclusion, LncRNA HOTAIR can regulate the ability of invasion and migration of endometrial stromal cells, and its mechanism is proved by regulating the miR-519b-3p/PRRG4 pathway.
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References (31)
- Endometrial stromal cell inflammatory phenotype during severe ovarian endometriosis as a cause of endometriosis-associated infertility via openalex
- Endometriosis: pathogenesis and treatment via openalex
- Eutopic and ectopic stromal cells from patients with endometriosis exhibit differential invasive, adhesive, and proliferative behavior via openalex
- Exosomal lncRNA HOTAIR Promotes the Progression and Angiogenesis of Endometriosis via the miR-761/HDAC1 Axis and Activation of STAT3-Mediated Inflammation via openalex
- Exosomal lncRNA HOTAIR Promotes the Progression and Angiogenesis of Endometriosis via the miR-761/HDAC1 Axis and Activation of STAT3-Mediated Inflammation via openalex
- Genetic impacts on thermostability of onco-lncRNA HOTAIR during the development and progression of endometriosis via openalex
- Genome-wide profiling of long noncoding ribonucleic acid expression patterns in ovarian endometriosis by microarray via openalex
- H19 lncRNA alters stromal cell growth via IGF signaling in the endometrium of women with endometriosis via openalex
- Hypothetical roadmap towards endometriosis: prenatal endocrine-disrupting chemical pollutant exposure, anogenital distance, gut-genital microbiota and subclinical infections via openalex
- LINC00261 functions as a competing endogenous RNA to regulate BCL2L11 expression by sponging miR-132-3p in endometriosis. via openalex
- PPARγ Agonists: Emergent Therapy in Endometriosis via openalex
- W2936030917 via openalex
- W2944808099 via openalex
- W2964318180 via openalex
- W2971126595 via openalex
- W2765750028 via openalex
- W2991402734 via openalex
- W3005525923 via openalex
- W2419326786 via openalex
- W3023899890 via openalex
- W2136222002 via openalex
- W3092312312 via openalex
- W3108443692 via openalex
- W3123590586 via openalex
- W2109420358 via openalex
- W2040831013 via openalex
- W4220750323 via openalex
- W1982313475 via openalex
- W6717261607 via openalex
- W2799524602 via openalex
- W6770426139 via openalex
Cited by (13)
- ASPM promotes the progression of ovarian endometriosis by modulating the cell cycle and activating the Wnt/β-catenin signaling pathway 2026
- Leveraging epigenetic aberrations in the pathogenesis of endometriosis: from DNA methylation to non-coding RNAs 2025
- An overview of endometriosis and molecular target-based therapeutic approach 2025
- LINC01638 promotes epithelial-to-mesenchymal transition in endometriosis epithelial cells by up-regulating RHOB via HDAC1 suppression 2025
- The Survey of long non-coding RNA HOTTIP expression level in endometriosis 2025
- The role of long non-coding ribonucleic acid HOXA11-AS in endometriosis therapy 2025
- Apparent lncRNAs involvement in pathogenesis of endometriosis 2024
- The roles of chromatin regulatory factors in endometriosis 2024
- Chromatin modifiers in endometriosis pathogenesis 2024
- Liquid Biopsy in Endometriosis: A Systematic Review 2023
- Hypomethylation of the <i>ENPP3</i> promoter region contributes to the occurrence and development of ovarian endometriosis via the AKT/mTOR/4EBP1 signaling pathway 2023
- ITCH-Mediated Ubiquitylation of ITGB3 Promotes Cell Proliferation and Invasion of Ectopic Endometrial Stromal Cells in Ovarian Endometriosis 2023
- Analysis of lcnRNA Homebox Transcript antisense RNA (HOTAIR) expression in Polish Women with Endometriosis 2023
Source provenance
- europepmc
- last seen: 2026-06-12T06:13:51.797165+00:00
- openalex
- last seen: 2026-06-10T17:14:06.276822+00:00
- pubmed
- last seen: 2026-06-11T06:19:14.295875+00:00
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