ArticleClinical science (London, England : 1979)2024
Targeting the long non-coding RNA MIAT for the treatment of fibroids in an animal model.
Article in Clinical science (London, England : 1979), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed.
- A Comparative Analysis of the Methylation Status of Non-Coding RNA Promoters in Fibroid and Matched Myometrium.International journal of molecular sciences · 2026Article
- Transcriptomic and functional analysis of fibroid extracellular vesicles.Clinical science (London, England : 1979) · 2026Article
- Liquid Biopsy in Uterine Leiomyosarcoma: Current Biomarkers, Emerging Technologies, and Future Perspectives.Current oncology reports · 2026Review
- MIAT: An important long non-coding RNA regulating cardiovascular and cerebrovascular diseases.Frontiers in cardiovascular medicine · 2026Review
- Review
- Review
- Comparative Analysis of Differentially Expressed Long Non-Coding RNA in Pre- and Postmenopausal Fibroids.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
- The Functional Role of the Long Non-Coding RNA LINCMD1 in Leiomyoma Pathogenesis.International journal of molecular sciences · 2024Article
- In Vivo Effects of Bay 11-7082 on Fibroid Growth and Gene Expression: A Preclinical Study.Cells · 2024Article
- Regulatory effect of N6-methyladenosine on tumor angiogenesis.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Our previous studies indicated that there is overexpression of MIAT in fibroids and MIAT is a sponge for the miR-29 family in these tumors. The objective of the present study was to determine if the knockdown of MIAT in fibroid xenografts will increase miR-29 levels and reduce the expression of genes targeted by this miRNA such as collagen and cell cycle regulatory proteins in a mouse model for fibroids. Ovariectomized CB-17 SCID/Beige mice bearing estrogen/progesterone pellets were implanted subcutaneously in the flank with equal weight of fibroid explants which had been transduced by lentivirus for either control (empty vector) or MIAT knockdown for four weeks (n=7). Knockdown of MIAT in fibroid xenografts resulted in a 30% reduction of tumor weight and a marked increase in miR-29a, -b, and -c levels in the xenografts. There was reduced cell proliferation and expression of cell cycle regulatory genes CCND1, CDK2, and E2F1 and no significant changes in apoptosis. The xenografts with MIAT knockdown expressed lower mRNA and protein levels of FN1, COL3A1, and TGF-β3, and total collagen protein. Targeting MIAT, which sponges the pro-fibrotic miR-29 family, is an effective therapy for fibroids by reducing cell proliferation and thereby, tumor growth and accumulation of ECM, which is a hallmark of these benign gynecologic tumors.
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