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Studies have demonstrated that several cytokines are associated with the evolution of endometriosis, including tumor necrosis factor-\u03b1 (TNF\u03b1). TNF\u03b1 is a non-glycosylated cytokine protein with potent inflammatory, cytotoxic, and angiogenic potential. In the current study, we examined the ability of TNF\u03b1 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 TNF\u03b1-treated NESCs. The phosphorylation of the pro-inflammatory molecule NF-\u03baB and the candidates of the survival pathways PI3K, AKT, and ERK was measured by western blot analysis. The elevated secretion of TNF\u03b1 in EESCs downregulates the expression level of several miRNAs significantly in EESCs compared to NESCs. Also, treatment of NESCs with exogenous TNF\u03b1 significantly reduced the expression of miRNAs in a dose-dependent manner to levels similar to EESCs. In addition, TNF\u03b1 significantly increased the phosphorylation of the PI3K, AKT, ERK, and NF-\u03baB 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 TNF\u03b1 is upregulated in EESCs, which subsequently dysregulates the expression of miRNAs, contributing to the pathophysiology of endometriotic cells. CUR effectively inhibits the expression of TNF\u03b1, subsequently altering miRNA levels and suppressing the phosphorylation of AKT, ERK, and NF-\u03baB.<\/jats:p>","DOI":"10.1007\/s10753-023-01862-x","type":"journal-article","created":{"date-parts":[[2023,6,30]],"date-time":"2023-06-30T03:02:36Z","timestamp":1688094156000},"page":"2055-2070","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":29,"title":["TNF\u03b1-Induced Altered miRNA Expression Links to NF-\u03baB Signaling Pathway in Endometriosis"],"prefix":"10.1007","volume":"46","author":[{"given":"Saswati","family":"Banerjee","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Xu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aaron","family":"Doctor","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adel","family":"Driss","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ceana","family":"Nezhat","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Neil","family":"Sidell","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert N.","family":"Taylor","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Winston E.","family":"Thompson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Indrajit","family":"Chowdhury","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2023,6,30]]},"reference":[{"issue":"13","key":"1862_CR1","doi-asserted-by":"publisher","first-page":"1244","DOI":"10.1056\/NEJMra1810764","volume":"382","author":"KT Zondervan","year":"2020","unstructured":"Zondervan, K.T., C.M. 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