MicroRNA‑16 inhibits endometrial stromal cell migration and invasion through suppression of the inhibitor of nuclear factor‑κB kinase subunit β/nuclear factor‑κB pathway
- Xiaoping Wang
- Rui Ren
- Meili Shao
- Jun Lan
Affiliations: Department of Reproductive Medicine, The Second Hospital Affiliated to Lanzhou University, Lanzhou, Gansu 730030, P.R. China, Department of Obstetrics and Gynecology, The People's Hospital of Gansu, Lanzhou, Gansu 730000, P.R. China, Department of Obstetrics and Gynecology, The Women and Children Hospital of Shaanxi Province, Xi'an, Shaanxi 710061, P.R. China, Department of Gynecology, The Maternal and Child Care Service Center of Dongguan City Guangdong Province, Dongguan, Guangdong 523120, P.R. China
- Published online on: May 29, 2020 https://doi.org/10.3892/ijmm.2020.4620
Copyright: © Wang
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Accumulating evidence has demonstrated that endometrial stromal cells (ESCs) are responsible for the pathogenesis of endometriosis (Ems), which is characterized by the presence of functional endometrial‑like tissues outside the uterine cavity. Abnormal expression of microRNAs (miRNAs) in ESCs may be implicated in the etiology of Ems; however, the exact mechanisms have yet to be fully elucidated. The aim of the present study was to investigate the effects of miRNAs on ESCs and the underlying mechanisms. Using a microarray assay, microRNA‑16 (miR‑16) was found to be significantly downregulated in the ectopic endometrial tissues in patients with Ems, compared with that in eutopic endometrial tissues. Overexpression of miR‑16 significantly suppressed the migration and invasion of ESCs, whereas miR‑16 inhibition exerted the opposite effects. Furthermore, dual luciferase reporter assay demonstrated that miR‑16 directly targeted the inhibitor of nuclear factor (NF)‑κB kinase subunit β (IKKβ) and suppressed its translation. It was observed that the expression of IKKβ was upregulated and inversely correlated with miR‑16 levels in the ectopic endometrial tissues in patients with Ems. Additionally, knockdown of IKKβ by si‑IKKβ mimicked the effects of miR‑16 overexpression on ESCs, while the promoting effects of IKKβ overexpression on the migration and invasion of ESCs were attenuated by miR‑16 overexpression. Finally, miR‑16 inhibited the activation of the NF‑κB pathway by targeting IKKβ. Collectively, these results demonstrated that miR‑16 may suppress Ems by inhibiting the IKKβ/NF‑κB pathway, suggesting that miR‑16 may be a useful target in the treatment of Ems.