Archives of biochemistry and biophysics · 2026
LncRNA MALAT1 affects the progression of endometritis induced by lipopolysaccharide via regulating the expression of miR-142-3p.
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Chen Honglei, Huang Yuzhen, Yang Chenxi, Lu Xuan, Song Jialun, Liu Feifei, Han Ting
Аннотация
BACKGROUND: Chronic endometritis (CE) is a common gynecological disorder linked to infertility, but its pathogenesis remains unclear.
AIM: To investigate the role of lncRNA MALAT1 in lipopolysaccharide (LPS)-induced endometritis and its regulatory mechanism involving the miR-142-3p/PIK3R1 axis.
METHODS: A total of 133 patients with chronic endometritis (CE) and 100 healthy controls were enrolled. Serum and endometrial tissue samples were collected to detect the expression levels of MALAT1, miR-142-3p, and PIK3R1 using RT-qPCR. LPS-treated human endometrial stromal cells (HESCs) were used to establish an endometritis cell model. Cell transfection with MALAT1 siRNA, miR-142-3p mimic/inhibitor, and their negative controls was performed. ELISA was used to measure the concentrations of IL-6, IL-1β, and TNF-α. The CCK-8 assay assessed cell viability. Bioinformatics tools (lncLocator, Starbase, STRING) and dual-luciferase reporter assay validated the targeting relationships among MALAT1, miR-142-3p, and PIK3R1. Western blot assay was performed to measure the protein expression of PIK3R1 and PI3K/Akt pathway.
RESULTS: MALAT1 and PIK3R1 were upregulated in serum and tissues of CE patients, while miR-142-3p was downregulated. MALAT1 had certain diagnostic value for distinguishing CE from healthy controls. LPS treatment induced inflammatory responses in HESCs, and knockdown of MALAT1 inhibited LPS-induced overexpression of IL-6, IL-1β, and TNF-α. Mechanistically, MALAT1 directly targeted miR-142-3p, and miR-142-3p targeted PIK3R1. Co-transfection of si-MALAT1 and miR-142-3p inhibitor partially reversed the anti-inflammatory effect of MALAT1 knockdown by regulating PI3K/Akt pathway.
CONCLUSION: MALAT1 promotes LPS-induced endometritis progression by modulating miR-142-3p to upregulate PIK3R1, suggesting the MALAT1/miR-142-3p/PIK3R1 axis as a potential diagnostic indicator and therapeutic target for CE.
AIM: To investigate the role of lncRNA MALAT1 in lipopolysaccharide (LPS)-induced endometritis and its regulatory mechanism involving the miR-142-3p/PIK3R1 axis.
METHODS: A total of 133 patients with chronic endometritis (CE) and 100 healthy controls were enrolled. Serum and endometrial tissue samples were collected to detect the expression levels of MALAT1, miR-142-3p, and PIK3R1 using RT-qPCR. LPS-treated human endometrial stromal cells (HESCs) were used to establish an endometritis cell model. Cell transfection with MALAT1 siRNA, miR-142-3p mimic/inhibitor, and their negative controls was performed. ELISA was used to measure the concentrations of IL-6, IL-1β, and TNF-α. The CCK-8 assay assessed cell viability. Bioinformatics tools (lncLocator, Starbase, STRING) and dual-luciferase reporter assay validated the targeting relationships among MALAT1, miR-142-3p, and PIK3R1. Western blot assay was performed to measure the protein expression of PIK3R1 and PI3K/Akt pathway.
RESULTS: MALAT1 and PIK3R1 were upregulated in serum and tissues of CE patients, while miR-142-3p was downregulated. MALAT1 had certain diagnostic value for distinguishing CE from healthy controls. LPS treatment induced inflammatory responses in HESCs, and knockdown of MALAT1 inhibited LPS-induced overexpression of IL-6, IL-1β, and TNF-α. Mechanistically, MALAT1 directly targeted miR-142-3p, and miR-142-3p targeted PIK3R1. Co-transfection of si-MALAT1 and miR-142-3p inhibitor partially reversed the anti-inflammatory effect of MALAT1 knockdown by regulating PI3K/Akt pathway.
CONCLUSION: MALAT1 promotes LPS-induced endometritis progression by modulating miR-142-3p to upregulate PIK3R1, suggesting the MALAT1/miR-142-3p/PIK3R1 axis as a potential diagnostic indicator and therapeutic target for CE.