TRIM65 Promotes Invasion of Endometrial Stromal Cells by Activating ERK1/2/C-myc Signaling via Ubiquitination of DUSP6

Ying-Ting Wu, Yingting Wu, Siyu Ma, Si-Yu Ma, Wenqin Sun, Wen-Qin Sun, Weiwei Shen, Wei-Wei Shen, Huiting Zhu, Hui-Ting Zhu, Qin Zhang, Huifen Chen, Hui-Fen Chen
The Journal of clinical endocrinology and metabolism · 2020 · vol. 106(2) , pp. 526–538 · doi:10.1210/clinem/dgaa804 · PMID:33146694 · W3096467459
article OA: bronze CC0 ⤵ 28 in-corpus citations
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TRIM65 promotes endometrial stromal cell invasion by ubiquitylating DUSP6, activating ERK1/2/C-myc signaling, and establishing a feedback loop.

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Abstract

BACKGROUND: Endometriosis (EM) is a benign gynecological disease that shares some characteristics with malignancy, such as proliferation and invasion. So far, the pathogenesis of EM is still unclear. In this study, we investigated whether TRIM65 can play a role in the development of EM. METHODS: TRIM65 expression levels in eutopic, ectopic, and normal endometrium were detected by quantitative real-time PCR and Western blot. Cell proliferation and invasion of primary endometrial stromal (EMS) cells were detected by CCK-8 and Transwell analysis. The interaction between TRIM65 and DUSP6 or C-myc was measured by coimmunoprecipitation, ubiquitylation, dual luciferase, and chromatin immunoprecipitation analysis. RESULTS: We found that TRIM65 was identified as an up-regulated gene in ectopic endometrial tissues and EMS cells compared with control groups without EM. TRIM65 expression was positively correlated with the levels of p-ERK1/2, C-myc, matrix metalloproteinase-2, and integrin β1 in ectopic endometrial tissues in patients and mice. TRIM65 promoted the cell proliferation and invasion of EMS cells via the ERK1/2/C-myc pathway through ubiquitination of DUSP6. C-myc promoted TRIM65 expression through inducing TRIM65 promoter activity. Additionally, the increased expression of TRIM65, C-myc, matrix metalloproteinase-2, integrin β1, and p-ERK1/2 and the decreased expression of DUSP6 in ectopic endometrial tissues were significantly suppressed by inhibition of ERK1/2 signaling pathway in ectopic endometrial tissues in experimental mice model. CONCLUSION: In conclusion, TRIM65 promotes invasion of ectopic EMS cells by activating a feedback loop with the ERK1/2/C-myc signaling pathway and may be a potential therapeutic target for EM.

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Condition tags

endometriosis

MeSH descriptors

Dual Specificity Phosphatase 6 Endometriosis Endometrium Gene Expression Regulation Tripartite Motif Proteins Ubiquitination Ubiquitin-Protein Ligases Adult Animals Case-Control Studies Cell Movement Cell Proliferation Dual Specificity Phosphatase 6 Dual Specificity Phosphatase 6 Endometriosis Endometriosis Endometriosis Endometrium Endometrium Female

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