LncRNA LUCAT1 Promotes the Pathogenesis of Intrauterine Adhesion by Regulating AREG
10.11969/j.issn.1673-548X.2024.05.019
- VernacularTitle:lncRNA LUCAT1调控AREG的表达促进宫腔粘连的发生
- Author:
Jianhong WU
1
;
Yucui TIAN
;
Zi-Wen JIANG
Author Information
1. 100026 首都医科大学附属北京妇产医院/北京妇幼保健院妇科
- Keywords:
Intrauterine adhesion;
Epithelial-to-mesenchymal transition;
LncRNA;
LUCAT1;
AREG
- From:
Journal of Medical Research
2024;53(5):92-98
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of long non-coding RNA(lncRNA)lung cancer-related transcript 1(LUCAT1)on the pathogenesis of intrauterine adhesion by regulating the expression of amphiregulin(AREG),to provide a new molecular target for the prevention and treatment of intrauterine adhesions.Methods Real-time quantitative polymerase chain reaction(RTqPCR)was used to determine the mRNA expression levels of lncRNA LUCAT1,fibrotic markers of α-smooth muscle actin(α-SMA)and collagen type Ⅰ alpha 1 chain protein(COL1A1)in samples of intrauterine adhesion tissue and endometrial stromal cell treated with transforming growth factor-β1.Western blot was used to determine the protein expression levels of AREG,α-SMA,COL1A1.Then,si-LUCAT1,pcDNA LUCAT1,si-AREG were transfected into ESC and RT-qPCR was used to detect the mRNA expression levels of lncRNA LUC-AT1 and AREG.Next,si-LUCAT1 and pcDNA LUCAT1 were transfected into ESC and treated these cells with TGF-β1 for 48h,re-spectively.Western blot was used to further detect the protein expression levels of AREG,α-SMA and COL1A1,and cell proliferation and apoptosis were detected by cell proliferation assay and cell apoptosis assay.Results The expression levels of lncRNA LUC AT1,AR-EG and fibrosis markers α-SMA and COL1A1 were upregulated in endometrial tissues from patients with intrauterine adhesion and in ESC that had been treated with TGF-β1.AREG changed with the change of lncRNA LUCAT1,and the expression of lncRNA LUC-AT1did not change significantly after downregulation of AREG,and AREG was positively regulated by lncRNA LUCAT1.During the process of the transformation of ESC into fibroblasts,si-LUCAT1 significantly inhibited the protein expression levels of AREG,α-SMA and COL1A1(P＜0.01),significantly reduced cell proliferation and significantly induced cell apoptosis,the difference was statistically significant(P＜0.001).pcDNA LUCAT1 significantly induced the protein expression levels of AREG,α-SMA and COL1A1,and the difference was statistically significant(P＜0.01).Conclusion LncRNA LUCAT1 promotes the pathogenesis of intrauterine adhesion by up-regulating the expression of AREG.LncRNA LUCAT1/AREG axis may provide novel molecular target for the prevention and treat-ment of intrauterine adhesion.
