RAS/MEK/ERK Signal Pathway Regulates NF-κBp65 to Promote the Invasion and Proliferation of Endometrial Stromal Cells in Endometriosis

Meng Wei, Fang Wang, Lihong Shang, Ting Hao, Yu e Yang, Chunfang Ha
In: JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS · 2022 · vol. 36(3) · doi:10.23812/j.biol.regul.homeost.agents.20223603.55 · W4407306770
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This study found that the RAS/MEK/ERK signaling pathway upregulates NF-κBp65, promoting proliferation and invasion in endometrial stromal cells from endometriosis patients.

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This prospective case-control study examined expression of the RAS/MEK/ERK pathway components (RAS, MEK, ERK) and NF-κB p65 in endometrial tissues from 15 patients, comparing eutopic/ectopic endometrial stromal contexts and endometriotic ovarian cyst wall with endometrium from controls and non-endometriotic ovarian cyst wall. The study found significantly higher levels of RAS, MEK, ERK, and NF-κBp65 in endometriosis-associated stromal cells, and silencing MEK, ERK, or NF-κBp65 suppressed endometrial stromal cell proliferation and invasion as measured by CCK-8 and Trans-well. Western blot results supported an upstream-to-downstream relationship in which NF-κBp65 protein decreased after ERK/MEK/RAS/MEK/ERK pathway suppression, while RAS, MEK, and ERK expression did not change after NF-κBp65 knockdown. This paper is centrally about endometriosis — it investigates RAS/MEK/ERK-driven regulation of NF-κB p65 to promote proliferation and invasion of endometrial stromal cells.

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Abstract

Objectives: The aim of this study is to investigate the relationship between the Nuclear factor-kappa B (NF-κBp65) and RAS/MEK/ERK signaling cascade and their influence on the proliferation and invasion of endometrial stromal cells. Design: A prospective case control study was carried out. The endometriotic ovarian cyst wall was examined as a case whereas endometrial tissue obtained during endometrial curettage and non-endometriotic ovarian cyst wall were examined as controls (n = 15). Methods: To explore the relationship between RAS/MEK/ERK and NF-κB pathway, we firstly detected the expression of RAS, MEK, ERK and NF-κBp65 in the control endometrium and eutopic/ectopic endometrium with endometriosis. Then their affection on the proliferative and invasive abilities of endometrial stromal cells was analyzed by CCK-8 and Trans-well and verified the upstream and downstream relationship between RAS/MEK/ERK and NF-κB signaling pathway cascade by Western blot. Results: The results revealed that the expression levels of MAPK kinase-dependent molecules RAS, MEK, ERK and NF-κBp65 in eutopic/ectopic endometrial stromal cells of patients with endometriosis were significantly higher than those in the control group ( p < 0.05). When the expression of MEK, ERK and NF-κBp65 were respectively silenced, the proliferation and invasion of eutopic endometrial stromal cells were all significantly suppressed. They all participated in the progress of endometriosis. Of note, the expression of NF-κBp65 protein was obviously inhibited after respectively suppressing ERK, MEK and RAS/MEK/ERK signaling pathway ( p 0.05). Conclusions: The NF-κBp65 is regulated by the RAS/MEK/ERK signal pathway to promote the proliferation and invasion of eutopic endometrial stromal cells. Its inhibitors provide the selection of multiple potential targets and different joint intervention approaches for non-hormonal therapy for endometriosis.
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Abstract

Objectives: The aim of this study is to investigate the relationship between the Nuclear factor-kappa B (NF-κBp65) and RAS/MEK/ERK signaling cascade and their influence on the proliferation and invasion of endometrial stromal cells. Design: A prospective case control study was carried out. The endometriotic ovarian cyst wall was examined as a case whereas endometrial tissue obtained during endometrial curettage and non-endometriotic ovarian cyst wall were examined as controls (n = 15). Methods: To explore the relationship between RAS/MEK/ERK and NF-κB pathway, we firstly detected the expression of RAS, MEK, ERK and NF-κBp65 in the control endometrium and eutopic/ectopic endometrium with endometriosis. Then their affection on the proliferative and invasive abilities of endometrial stromal cells was analyzed by CCK-8 and Trans-well and verified the upstream and downstream relationship between RAS/MEK/ERK and NF-κB signaling pathway cascade by Western blot. Results: The results revealed that the expression levels of MAPK kinase-dependent molecules RAS, MEK, ERK and NF-κBp65 in eutopic/ectopic endometrial stromal cells of patients with endometriosis were significantly higher than those in the control group (p < 0.05). When the expression of MEK, ERK and NF-κBp65 were respectively silenced, the proliferation and invasion of eutopic endometrial stromal cells were all significantly suppressed. They all participated in the progress of endometriosis. Of note, the expression of NF-κBp65 protein was obviously inhibited after respectively suppressing ERK, MEK and RAS/MEK/ERK signaling pathway (p 0.05). Conclusions: The NF-κBp65 is regulated by the RAS/MEK/ERK signal pathway to promote the proliferation and invasion of eutopic endometrial stromal cells. Its inhibitors provide the selection of multiple potential targets and different joint intervention approaches for non-hormonal therapy for endometriosis.

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References Supporting Agencies Copyright (c) 2022 Meng Wei, Fang Wang, Lihong Shang, Ting Hao, Yu e Yang, Chunfang Ha This site is licensed under a Creative Commons Attribution 4.0 International License (CC BY 4.0). Medical Genetics, University of Torino Medical School, Italy Department of Biomedical, Surgical and Dental Sciences, University of Milan, Italy

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