Effect of LncRNA SNHG16 targeting miR-141-3p/HMGB1 axis on angiogenesis of endometrial stromal cells in ectopic adenomyosis
10.19405/j.cnki.issn1000–1492.2026.03.020
- VernacularTitle:LncRNA SNHG16靶向miR-141-3p/HMGB1轴对子宫腺肌病异位子宫内膜间质细胞血管生成的影响
- Author:
Ting LIU
1
;
Mingyang WANG
1
;
Xiaofeng ZOU
1
Author Information
1. Gynecology Department of Zunyi Medical University Affiliated Hospital，Zunyi 563000
- Publication Type:Journal Article
- Keywords:
adenomyosis;
ectopic endometrial stromal cells;
LncRNA SNHG16;
miR-141-3p;
HMGB1;
angiogenesis
- From:
Acta Universitatis Medicinalis Anhui
2026;61(3):533-539
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the effect of interfering with long noncoding RNA （LncRNA） small nucleolar RNA host gene16 （SNHG16） on improving angiogenesis of ectopic endometrial stromal cells （EScs） in adenomyosis （AM） by targeting upregulation of miRNA （miR）-141-3p and inhibition of high mobility group box-1 protein （HMGB1）. MethodsThe expression levels of SNHG16， miR-141-3p and HMGB1 mRNA in endometrial tissues of 52 patients with adenomyosis （AM group） and 52 patients who needed hysterectomy due to cervical cancer or ovarian cancer （control group） were detected by quantitative reverse transcription polymerase chain reaction （qRT-PCR）. Y14 cells were divided into small hairpin RNA （shRNA） NC group， shRNA SNHG16 group， shRNA SNHG16+miR-141-3p inhibitor （inhibitor） group， shRNA SNHG16+inhibitor NC group and blank group. The targeting relationship between miR-141-3p and SNHG16 as well as HMGB1 was verified. The expression levels of SNHG16， miR-141-3p and HMGB1 mRNA in Y14 cells were detected by qRT-PCR. CCK-8 and Transwell assay were used to detect cell proliferation， invasion and migration. Microvascular density （MVD） was determined by immunofluorescence. The expressions of hypoxia-inducing factor α （HIF-1α）， cyclooxygenase-2 （Cox-2）， vascular endothelial growth factor （VEGF） and HMGB1 were detected by Western blot. ResultsThe expression of SNHG16 and HMGB1 mRNA in AM group was higher than that in control group， but the expression of miR-141-3p was lower than that in control group （P0.05）. The expression of SNHG16， HMGB1 mRNA， proliferation rate， migration， invasion number， MVD， expression of VEGF， HIF-1 α， Cox-2， and HMGB1 proteins in the shRNA SNHG16 group were lower than those in the blank group and shRNA NC group， while the expression of miR-141-3p was higher than that in the blank group and shRNA NC group （P0.05）. Inhibition of miR-141-3p reversed the improvement of EScs angiogenesis by interfering with SNHG16. ConclusionInterference with LncRNA SNHG16 improves EScs angiogenesis and inhibits proliferation， migration， and invasion of EScs by targeting upregulation of miR-141-3p and inhibition of HMGB1.
