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Updated: Jan 20, 2026
Long Non-coding RNAs: Chromatin Modification, Cell Differentiation & Immune Response
Effects of lncRNA BANCR on endometriosis through ERK/MAPK pathway
1Department of Gynecology, Ningbo Women and Children's Hospital, Ningbo, China. zhuminbo@163.com.
Objective:
To investigate the regulatory role of long non-coding ribonucleic acid (lncRNA) BRAF-activated non-coding RNA (BANCR) in rats with endometriosis (EMs) and its mechanism of action.
Materials And Methods:
A total of 30 healthy, unmated, female Sprague-Dawley (SD) rats were selected and divided into sham-operation group, model group and lncRNA BANCR intervention group, and a rat model of EMs was established by means of autotransplantation. The volume of eutopic endometrium in each group of rats was measured, and hematoxylin and eosin (HE) staining was applied to detect the impacts on the pathological morphology of ectopic endometrial tissues in each group. The levels of vascular endothelial growth factor (VEGF), matrix metalloproteinase-2 (MMP-2) and MMP-9 in the rat serum were determined by virtue of enzyme-linked immunosorbent assay (ELISA), reverse transcription-polymerase chain reaction (RT-PCR) was performed to measure the messenger RNA (mRNA) levels of extracellular signal-regulated kinase (ERK) and mitogen-activated protein kinase (MAPK) in the uterine tissues in each group of rats, and Western blotting assay was adopted to detect the levels of phosphorylated ERK and MAPK proteins in the rat uterine tissues in each group.
Results:
Compared with those in sham-operation group, the volume of eutopic endometrium in the rats was increased markedly, the pathological morphology was poorer, and the content of VEGF, MMP-2 and MMP-9 in the serum, the mRNA levels of ERK and MAPK in the uterine tissues, and the levels of phosphorylated ERK and MAPK proteins were elevated notably in model group. The rats in lncRNA BANCR intervention group had evidently decreased volume of eutopic endometrium, improved pathological morphology and significantly declined content of serum VEGF, MMP-2 and MMP-9, ERK and MAPK mRNA levels, and phosphorylated ERK and MAPK protein levels in the uterine tissues than those in model group.
Conclusions:
LncRNA BANCR inhibitor can repress the development of ectopic endometrial tissues by inhibiting the generation of angiogenic factors in the EMs focus, and its mechanism may be related to the inhibition on the ERK/MAPK signaling pathway.
Insights
Long non-coding RNA BANCR may inhibit endometriosis development by targeting the ERK/MAPK pathway, reducing ectopic tissue growth and angiogenic factors. This study investigated its regulatory role in a rat model.
Area of Science:
- Reproductive biology
- Molecular genetics
- Cell signaling
Background:
- Endometriosis (EMs) is a debilitating condition characterized by ectopic endometrial tissue growth.
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their roles in various biological processes, including disease pathogenesis.
- The specific role of lncRNA BRAF-activated non-coding RNA (BANCR) in endometriosis remains to be fully elucidated.
Purpose of the Study:
- To investigate the regulatory role of lncRNA BANCR in a rat model of endometriosis.
- To explore the underlying mechanism of lncRNA BANCR's action in endometriosis development.
- To assess the potential of lncRNA BANCR as a therapeutic target for endometriosis.
Main Methods:
- Establishment of a rat model of endometriosis via autotransplantation.
- Assessment of eutopic endometrium volume and pathological morphology of ectopic tissues.
- Quantification of serum vascular endothelial growth factor (VEGF), matrix metalloproteinase-2 (MMP-2), and MMP-9 levels using ELISA.
- Measurement of extracellular signal-regulated kinase (ERK) and mitogen-activated protein kinase (MAPK) mRNA and protein levels in uterine tissues via RT-PCR and Western blotting.
Main Results:
- Rats with endometriosis exhibited increased eutopic endometrium volume, poorer pathological morphology, and elevated serum VEGF, MMP-2, MMP-9, and uterine ERK/MAPK signaling.
- Intervention with a lncRNA BANCR inhibitor significantly reduced eutopic endometrium volume and improved pathological morphology.
- lncRNA BANCR inhibition led to decreased levels of serum VEGF, MMP-2, MMP-9, and suppressed uterine ERK/MAPK pathway activation.
Conclusions:
- lncRNA BANCR inhibitor effectively represses the development of ectopic endometrial tissues in endometriosis.
- The mechanism involves the inhibition of angiogenic factor generation within the endometriotic focus.
- lncRNA BANCR's therapeutic potential in endometriosis may be mediated through the regulation of the ERK/MAPK signaling pathway.
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