Effects of lncRNA BANCR on endometriosis through ERK/MAPK pathway.

Zhu MB, M.-B. Zhu, Chen LP, L-P Chen, M Hu, Hu M, Manli Hu, Shi Z, Zi-Gang Shi, Z Shi, Y-N Liu, Liu YN
European review for medical and pharmacological sciences · 2019 · vol. 23(16) , pp. 6806–6812 · doi:10.26355/eurrev_201908_18719 · PMID:31486479 · W2989689429
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-07 ⓘ

This study found that lncRNA BANCR inhibition repressed endometriosis development in rats by downregulating the ERK/MAPK signaling pathway and reducing angiogenic factors.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 · read from full text ⓘ

The study investigated whether inhibiting long non-coding RNA BANCR affects endometriosis in a rat model and examined potential mechanisms involving the ERK/MAPK signaling pathway. Using 30 female Sprague-Dawley rats, the authors created an endometriosis model via autotransplantation and compared a sham group, a model group, and a lncRNA BANCR intervention group, assessing eutopic endometrium volume and ectopic tissue pathology (HE staining), serum VEGF and MMP-2/MMP-9 (ELISA), and uterine ERK/MAPK mRNA and phosphorylated protein levels (RT-PCR and Western blotting). BANCR intervention reduced eutopic endometrium volume, improved pathological morphology, and decreased VEGF, MMP-2, MMP-9, ERK/MAPK mRNA, and phosphorylated ERK and MAPK compared with the model group. The paper explicitly frames the mechanism as inhibition of the ERK/MAPK pathway, and the limitation noted by its design is that it relies on an animal model rather than human data. This paper is centrally about endometriosis — it tests lncRNA BANCR inhibition’s effects on ectopic endometrial tissue development via ERK/MAPK signaling.

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Abstract

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.
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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. Free PDF DownloadThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License To cite this article M.-B. Zhu, L.-P. Chen, M. Hu, Z. Shi, Y.-N. Liu Effects of lncRNA BANCR on endometriosis through ERK/MAPK pathway Eur Rev Med Pharmacol Sci Year: 2019 Vol. 23 - N. 16 Pages: 6806-6812 DOI: 10.26355/eurrev_201908_18719 Publication History Published online: 28 Aug 2019

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Endometrium Extracellular Signal-Regulated MAP Kinases MAP Kinase Signaling System Proto-Oncogene Proteins B-raf RNA, Long Noncoding Animals Disease Models, Animal Endometriosis Endometriosis Endometriosis Endometrium Endometrium Extracellular Signal-Regulated MAP Kinases Female MAP Kinase Signaling System Matrix Metalloproteinase 2 Matrix Metalloproteinase 2 Matrix Metalloproteinase 9 Matrix Metalloproteinase 9

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