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

J. Yu, L.-H. Chen, B. Zhang, Q.-M. Zheng

Department of Obstetrics and Gynecology, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China. shangsuji737@163.com

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• Gynecology

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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