m6A methyltransferase METTL3 inhibits endometriosis by regulating alternative splicing of MIR17HG
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The m6A methyltransferase METTL3 inhibits endometriosis by upregulating MIR17HG expression, suppressing endometrial stromal cell proliferation, migration, invasion, and altering estradiol and lipoprotein levels.
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Abstract
IN BRIEF: Inflammation and abnormal immune response are the key processes in the development of endometriosis (EMs), and m6A modification can regulate the inflammatory response. This study reveals that METTL3-mediated N6-methyladenosine (m6A) modification plays an important role in EMs.
ABSTRACT: m6A modification is largely involved in the development of different diseases. This study intended to investigate the implication of m6A methylation transferase methyltransferase like 3 (METTL3) in EMs. EMs- and m6A-related mRNAs and long non-coding RNAs were identified through bioinformatics analysis. Next, EM mouse models established by endometrial autotransplantation and mouse endometrial stromal cell (mESC) were prepared and treated with oe-METTL3 or sh-MIR17HG for pinpointing the in vitro and in vivo effects of METTL3 on EMs in relation to MIR17HG through the determination of mESC biological processes as well as estradiol (E2) and related lipoprotein levels. We demonstrated that METTL3 and MIR17HG were downregulated in the EMs mouse model. Overexpression of METTL3 suppressed the proliferation, migration, and invasion of mESCs. In addition, METTL3 enhanced the expression of MIR17HG through m6A modification. Moreover, METTL3 could inhibit the E2 level and alter related lipoprotein levels in EMs mice through the upregulation of MIR17HG. The present study highlighted that the m6A methylation transferase METTL3 prevents EMs progression by upregulating MIR17HG expression.
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Cited by (12)
- Hypoxia-mediated epigenetic silencing of YTHDF2 promotes endometriosis progression via the NFE2L1-NF-κB axis 2026
- Decreased Glycolysis Due to Lactate Dehydrogenase A N6-Methyladenosine Methylation in Endometrium of Endometriosis Impairs Its Decidualization and Contributes to Related Infertility 2025
- Epigenetics of endometriosis 2025
- Integrated Proteomics Reveals Spliceosome Dysregulation and Highlights DHX9 as a TGF-β Signaling-Driven Fibrosis Hub in Endometriosis 2025
- Advances in endometriosis research: animal models for the study of reproductive disorders 2025
- Inhibition of IGF2BP1 attenuates the progression of endometriosis through PTBP1 2024
- METTL3-dependent m6A modification facilitates decreased endometrial decidualization via attenuation of MET in endometriosis 2024
- Additional file 2 of METTL3-regulated m6A modification impairs the decidualization of endometrial stromal cells by regulating YTHDF2-mediated degradation of FOXO1 mRNA in endometriosis-related infertility 2024
- Additional file 2 of METTL3-regulated m6A modification impairs the decidualization of endometrial stromal cells by regulating YTHDF2-mediated degradation of FOXO1 mRNA in endometriosis-related infertility 2024
- METTL3-regulated m6A modification impairs the decidualization of endometrial stromal cells by regulating YTHDF2-mediated degradation of FOXO1 mRNA in endometriosis-related infertility 2023
- Additional file 1 of METTL3-regulated m6A modification impairs the decidualization of endometrial stromal cells by regulating YTHDF2-mediated degradation of FOXO1 mRNA in endometriosis-related infertility 2023
- Additional file 1 of METTL3-regulated m6A modification impairs the decidualization of endometrial stromal cells by regulating YTHDF2-mediated degradation of FOXO1 mRNA in endometriosis-related infertility 2023
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