TNFα-Induced Altered miRNA Expression Links to NF-κB Signaling Pathway in Endometriosis

Saswati Banerjee, Wei Xu, Aaron Doctor, Adel Driss, Ceana Nezhat, Neil Sidell, Robert N Taylor, Winston E Thompson, Indrajit Chowdhury
Inflammation · 2023 · vol. 46(6) , pp. 2055–2070 · doi:10.1007/s10753-023-01862-x · PMID:37389684 · PMC10673760 · W4382631077
article OA: gold CC0 ⤵ 10 in-corpus citations
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

TNFα in endometriosis upregulates NF-κB and related pathways while downregulating specific miRNAs, and curcumin treatment reverses these effects.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This study investigated whether TNFα alters microRNA (miRNA) expression linked to NF-κB-associated signaling in primary endometrial stromal cells, comparing eutopic endometrium from endometriosis subjects (EESC) with normal endometrial stromal cells (NESC) and using TNFα-treated NESCs as an in vitro model. Using RT-qPCR, the authors found that TNFα secretion-associated changes corresponded to significant downregulation of several miRNAs in EESC relative to NESC, and that exogenous TNFα reduced miRNA expression in a dose-dependent manner to levels similar to EESC; TNFα also increased phosphorylation of PI3K, AKT, ERK, and NF-κB signaling pathways. Curcumin treatment increased dysregulated miRNA expression in EESC in a dose-dependent way and was associated with reduced phosphorylation of these pathways, with the caveat that the work relies on in vitro cell models and selected measured miRNAs rather than a comprehensive in vivo assessment. This paper is centrally about endometriosis — it demonstrates TNFα-driven miRNA dysregulation linked to NF-κB/PI3K-AKT-ERK signaling in eutopic endometrial stromal cells and examines curcumin’s ability to modulate these changes.

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Abstract

Endometriosis is a common gynecological inflammatory disorder characterized by immune system dysregulation, which is involved in lesion initiation and progression. Studies have demonstrated that several cytokines are associated with the evolution of endometriosis, including tumor necrosis factor-α (TNFα). TNFα is a non-glycosylated cytokine protein with potent inflammatory, cytotoxic, and angiogenic potential. In the current study, we examined the ability of TNFα to induce dysregulation of microRNAs (miRNAs) linked to NFkB signaling pathways, thus contributing to the pathogenesis of endometriosis. Using RT-qPCR, the expression of several miRNAs was quantified in primary cells derived from eutopic endometrium of endometriosis subjects (EESC) and normal endometrial stromal cells (NESC), and also TNFα-treated NESCs. The phosphorylation of the pro-inflammatory molecule NF-κB and the candidates of the survival pathways PI3K, AKT, and ERK was measured by western blot analysis. The elevated secretion of TNFα in EESCs downregulates the expression level of several miRNAs significantly in EESCs compared to NESCs. Also, treatment of NESCs with exogenous TNFα significantly reduced the expression of miRNAs in a dose-dependent manner to levels similar to EESCs. In addition, TNFα significantly increased the phosphorylation of the PI3K, AKT, ERK, and NF-κB signaling pathways. Notably, treatment with curcumin (CUR, diferuloylmethane), an anti-inflammatory polyphenol, significantly increased the expression of dysregulated miRNAs in EESC in a dose-dependent manner. Our findings demonstrate that TNFα is upregulated in EESCs, which subsequently dysregulates the expression of miRNAs, contributing to the pathophysiology of endometriotic cells. CUR effectively inhibits the expression of TNFα, subsequently altering miRNA levels and suppressing the phosphorylation of AKT, ERK, and NF-κB.

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Condition tags

endometriosis

MeSH descriptors

Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin Curcumin

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