ArticlePloS one2013
MicroRNA-21 is induced by rapamycin in a model of tuberous sclerosis (TSC) and lymphangioleiomyomatosis (LAM).
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Epigenetic Insights into Tuberous Sclerosis Complex, Von Hippel-Lindau Syndrome, and Ataxia-Telangiectasia.Epigenomes · 2025Review
- The development for emerging biomarkers of lymphangioleiomyomatosis.Orphanet journal of rare diseases · 2024Review
- MicroRNA Expression Profile in TSC Cell Lines and the Impact of mTOR Inhibitor.International journal of molecular sciences · 2022Article
- Long-Term Effects of Sirolimus on Human Skin TSC2-Null Fibroblast‒Like Cells.The Journal of investigative dermatology · 2021Article
- High-throughput screening of circRNAs reveals novel mechanisms of tuberous sclerosis complex-related renal angiomyolipoma.Human genomics · 2021Article
- Article
- The Role of Non-Coding RNAs in Neurodevelopmental Disorders.Frontiers in genetics · 2019Review
- High-throughput chemical screening to discover new modulators of microRNA expression in living cells by using graphene-based biosensor.Scientific reports · 2018Article
- TSC2 regulates microRNA biogenesis via mTORC1 and GSK3β.Human molecular genetics · 2018Article
- Comparison of Cardiac miRNA Transcriptomes Induced by Diabetes and Rapamycin Treatment and Identification of a Rapamycin-Associated Cardiac MicroRNA Signature.Oxidative medicine and cellular longevity · 2018Article
- MicroRNA-induced silencing in epilepsy: Opportunities and challenges for clinical application.Developmental dynamics : an official publication of the American Association of Anatomists · 2018Review
- Emerging Role of mTOR Signaling-Related miRNAs in Cardiovascular Diseases.Oxidative medicine and cellular longevity · 2018Review
- mTORC1 suppresses PIM3 expression via miR-33 encoded by the SREBP loci.Scientific reports · 2017Article
- The Role of MicroRNAs in Cerebellar Development and Autism Spectrum Disorder During Embryogenesis.Molecular neurobiology · 2017Review
- Rapamycin-induced miR-21 promotes mitochondrial homeostasis and adaptation in mTORC1 activated cells.Oncotarget · 2017Article
- Synergistic treatment of TS.Oncotarget · 2017Article
- MicroRNA Transfer Between Bone Marrow Adipose and Multiple Myeloma Cells.Current osteoporosis reports · 2017Review
- MicroRNA profiling of low-grade glial and glioneuronal tumors shows an independent role for cluster 14q32.31 member miR-487b.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2017Article
- Rapamycin suppresses hypoxia/reoxygenation-induced islet injury by up-regulation of miR-21 via PI3K/Akt signalling pathway.Cell proliferation · 2017Article
- Abnormal serum microRNA profiles in tuberous sclerosis are normalized during treatment with everolimus: possible clinical implications.Orphanet journal of rare diseases · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Lymphangioleiomyomatosis (LAM), a multisystem disease of women, is manifest by the proliferation of smooth muscle-like cells in the lung resulting in cystic lung destruction. Women with LAM can also develop renal angiomyolipomas. LAM is caused by mutations in the tuberous sclerosis complex genes (TSC1 or TSC2), resulting in hyperactive mammalian Target of Rapamycin (mTOR) signaling. The mTOR inhibitor, Rapamycin, stabilizes lung function in LAM and decreases the volume of renal angiomyolipomas, but lung function declines and angiomyolipomas regrow when treatment is discontinued, suggesting that factors induced by mTORC1 inhibition may promote the survival of TSC2-deficient cells. Whether microRNA (miRNA, miR) signaling is involved in the response of LAM to mTORC1 inhibition is unknown. We identified Rapamycin-dependent miRNA in LAM patient angiomyolipoma-derived cells using two separate screens. First, we assayed 132 miRNA of known significance to tumor biology. Using a cut-off of >1.5-fold change, 48 microRNA were Rapamycin-induced, while 4 miRs were downregulated. In a second screen encompassing 946 miRNA, 18 miRs were upregulated by Rapamycin, while eight were downregulated. Dysregulation of miRs 29b, 21, 24, 221, 106a and 199a were common to both platforms and were classified as candidate "RapamiRs." Validation by qRT-PCR confirmed that these microRNA were increased. miR-21, a pro-survival miR, was the most significantly increased by mTOR-inhibition (p<0.01). The regulation of miR-21 by Rapamycin is cell type independent. mTOR inhibition promotes the processing of the miR-21 transcript (pri-miR-21) to a premature form (pre-miR-21). In conclusion, our findings demonstrate that Rapamycin upregulates multiple miRs, including pro-survival miRs, in TSC2-deficient patient-derived cells. The induction of miRs may contribute to the response of LAM and TSC patients to Rapamycin therapy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.