The modulation of endometriosis by lncRNA MALAT1 via NF-κB/iNOS

J Yu, Yu J, L-H Chen, Chen LH, Zhang B, B Zhang, Zheng QM, Q-M Zheng
European review for medical and pharmacological sciences · 2019 · vol. 23(10) , pp. 4073–4080 · doi:10.26355/eurrev_201905_17908 · PMID:31173276 · W2990409117
Lab / animal OA: closed CC0 ⤵ 13 in-corpus citations
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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-22 ⓘ

This study found that lncRNA MALAT1 is upregulated in endometriosis tissues and promotes endometrial cell proliferation and invasion by modulating MMP-9 expression through the NF-κB/iNOS pathway.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-22 · read from full text ⓘ

The paper studied whether the long non-coding RNA MALAT1 is differentially expressed in endometriosis and whether it affects endometrial cell behaviors through the NF-κB/iNOS signaling axis. Using real-time PCR, the authors compared MALAT1 levels in normal versus ectopic endometrial tissues, and in cultured endometrial cells they applied MALAT1 siRNA to assess effects on proliferation (MTT), invasion (Transwell), apoptosis-related caspase 3 activity, and protein expression of NF-κB/iNOS and MMP-9 by Western blot. MALAT1 was upregulated in ectopic tissues, and MALAT1 knockdown suppressed proliferation and invasion, increased caspase 3 activity, and reduced NF-κB/iNOS and MMP-9 expression. This paper is centrally about endometriosis — it reports that MALAT1 modulates endometriosis-related cell apoptosis and MMP-9 expression via NF-κB/iNOS.

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Abstract

OBJECTIVE: Endometriosis (Ems) is one benign disorder that frequently leads to chronic pelvic pain, dysmenorrhea or even infertility. Featured as the ectopic growth of active endometrial tissues on tissues beyond the muscular layer, Ems has complicated pathogenesis mechanisms that are not fully illustrated. Long non-coding (lnc) RNA MALAT1 participates in various biological activities, including cell growth, proliferation, apoptosis, organogenesis, inflammation, and tumors. However, its expression and function in Ems are not clear yet. PATIENTS AND METHODS: Real-time PCR measured differential expression of MALAT1 in normal and ectopic endometrial tissues. Cultured endometrial cells were transfected with siRNA for MALAT1, whose expression was measured by real-time PCR. MTT assay measured endometrial cell proliferation, whose invasion was measured by transwell assay. Western blot tested the expression and NF-κB/iNOS, and MMP9 proteins. RESULTS: LncRNA MALAT1 showed upregulation in ectopic endometrial tissues (p<0.05 comparing to control group). Transfection of MALAT1 siRNA suppressed its expression in endometrial cells, inhibited cell proliferation or invasion, enhanced caspase 3 activity, decreased NF-κB/iNOS or MMP-9 expression (p<0.05 comparing to control group). CONCLUSIONS: LncRNA MALAT1 can facilitate endometrial cell apoptosis and modulate MMP-9 expression via NF-κB/iNOS pathway, thus, mediating Ems pathogenesis.
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Objective

Endometriosis (Ems) is one benign disorder that frequently leads to chronic pelvic pain, dysmenorrhea or even infertility. Featured as the ectopic growth of active endometrial tissues on tissues beyond the muscular layer, Ems has complicated pathogenesis mechanisms that are not fully illustrated. Long non-coding (lnc) RNA MALAT1 participates in various biological activities, including cell growth, proliferation, apoptosis, organogenesis, inflammation, and tumors. However, its expression and function in Ems are not clear yet. PATIENTS AND METHODS: Real-time PCR measured differential expression of MALAT1 in normal and ectopic endometrial tissues. Cultured endometrial cells were transfected with siRNA for MALAT1, whose expression was measured by real-time PCR. MTT assay measured endometrial cell proliferation, whose invasion was measured by transwell assay. Western blot tested the expression and NF-κB/iNOS, and MMP9 proteins.

Results

LncRNA MALAT1 showed upregulation in ectopic endometrial tissues (p<0.05 comparing to control group). Transfection of MALAT1 siRNA suppressed its expression in endometrial cells, inhibited cell proliferation or invasion, enhanced caspase 3 activity, decreased NF-κB/iNOS or MMP-9 expression (p<0.05 comparing to control group).

Conclusions

LncRNA MALAT1 can facilitate endometrial cell apoptosis and modulate MMP-9 expression via NF-κB/iNOS pathway, thus, mediating Ems pathogenesis. This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License To cite this article J. Yu, L.-H. Chen, B. Zhang, Q.-M. Zheng The modulation of endometriosis by lncRNA MALAT1 via NF-κB/iNOS Eur Rev Med Pharmacol Sci Year: 2019 Vol. 23 - N. 10 Pages: 4073-4080 DOI: 10.26355/eurrev_201905_17908 Publication History Published online: 31 May 2019

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Condition tags

endometriosischronic_pelvic_paindysmenorrheainfertility

MeSH descriptors

Endometriosis NF-kappa B Nitric Oxide Synthase Type II RNA, Long Noncoding Adult Adult Apoptosis Apoptosis Apoptosis Cell Proliferation Cell Proliferation Cell Proliferation Endometriosis Endometriosis Female Female Humans Humans Matrix Metalloproteinase 9 Matrix Metalloproteinase 9

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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