ArticleFertility and sterility2019
Cross-talk between miR-29c and transforming growth factor-β3 is mediated by an epigenetic mechanism in leiomyoma.
Article in Fertility and sterility, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Transcriptomic and functional analysis of fibroid extracellular vesicles.Clinical science (London, England : 1979) · 2026Article
- Review
- Differential Expression of Small Non-Coding RNAs in Uterine Leiomyomas.International journal of molecular sciences · 2025Article
- The in vivo effects of knockdown of long non-coding RNA XIST on fibroid growth and gene expression.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Observational
- In Vivo Effects of Bay 11-7082 on Fibroid Growth and Gene Expression: A Preclinical Study.Cells · 2024Article
- Targeting the long non-coding RNA MIAT for the treatment of fibroids in an animal model.Clinical science (London, England : 1979) · 2024Article
- Therapeutic effects of in vivo administration of an inhibitor of tryptophan 2,3-dioxygenase (680c91) for the treatment of fibroids: a preclinical study.Fertility and sterility · 2024Article
- The Effect of Race/Ethnicity and MED12 Mutation on the Expression of Long Non-Coding RNAs in Uterine Leiomyoma and Myometrium.International journal of molecular sciences · 2024Article
- Therapeutic Effects of Long-Term Administration of Tranilast in an Animal Model for the Treatment of Fibroids.International journal of molecular sciences · 2023Article
- A View on Uterine Leiomyoma Genesis through the Prism of Genetic, Epigenetic and Cellular Heterogeneity.International journal of molecular sciences · 2023Review
- Differential Expression of MED12-Associated Coding RNA Transcripts in Uterine Leiomyomas.International journal of molecular sciences · 2023Article
- Differential Expression of Super-Enhancer-Associated Long Non-coding RNAs in Uterine Leiomyomas.Reproductive sciences (Thousand Oaks, Calif.) · 2022Article
- Long Noncoding RNA MIAT Modulates the Extracellular Matrix Deposition in Leiomyomas by Sponging MiR-29 Family.Endocrinology · 2021Article
- Tryptophan catabolism is dysregulated in leiomyomas.Fertility and sterility · 2021Article
- The Effect of Twisted Uterus Caused by Endometriosis or Myomatosis on Reproductive Treatment Outcomes.Journal of family & reproductive health · 2021Article
- The function role and synergic effect of syndecan-1 for mifepristone in uterine leiomyoma.Cytotechnology · 2021Article
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2 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo determine the expression of miR-29c and its target gene transforming growth factor-β3 (TGF-β3) in leiomyoma and the mechanisms of their reciprocal regulation.
designExperimental study.
settingAcademic research laboratory. PATIENT(S): Women undergoing hysterectomy for leiomyoma. INTERVENTION(S): Overexpression and underexpression of miR-29c; blockade of DNA methyltransferase 1 (DNMT1). MAIN OUTCOME MEASURE(S): The miR-29c and its target gene TGF-β3 in leiomyoma and the effects of TGF-β3 and blockade of DNMT1 on miR-29c expression. RESULT(S): Leiomyoma expressed significantly lower levels of miR-29c, but higher expression of TGF-β3 compared with matched myometrium. The expression of TGF-β3 and miR-29c were independent of race/ethnicity. Using 3' untranslated region luciferase reporter assay we confirmed that TGF-β3 is a direct target of miR-29c in leiomyoma smooth muscle cells (LSMCs). Gain-of-function of miR-29c in LSMCs inhibited the expression of TGF-β3 at protein and messenger RNA levels, whereas loss-of-function of miR-29c had the opposite effect. Treatment of LSMCs with TGF-β3 inhibited the expression of miR-29c, whereas it stimulated DNMT1 expression. Knockdown of DNMT1 through transfection with small interfering RNA significantly decreased the expression of TGF-β3, and induced miR-29c expression. Knockdown of DNMT1 also attenuated the inhibitory effect of TGF-β3 on miR-29c expression. Furthermore, we demonstrated that TGF-β3 increased the methylation level of miR-29c promoter in LSMCs. CONCLUSION(S): There is an inverse relationship in the expression of TGF-β3 and miR-29c in leiomyoma. The TGF-β3 is a direct target of miR-29c and inhibits the expression of miR-29c through an epigenetic mechanism. The cross-talk between miR-29c and TGF-β3 provides a feed forward mechanism of fibrosis in leiomyoma.
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