ArticleCell cycle (Georgetown, Tex.)2015
SMYD1 and G6PD modulation are critical events for miR-206-mediated differentiation of rhabdomyosarcoma.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 50 citations in OpenAlex.
- lncRNA Gm10451 mediates β-cell functional impairment in type 1 diabetes through the miR-24-3p/G6PD axis.Endocrine · 2026Article
- Histone methyltransferase SMYD1: playing a crucial role in disease progression.Frontiers in molecular biosciences · 2026Review
- MicroRNAs and angiosarcoma: are there promising reports?Frontiers in oncology · 2024Review
- Article
- MicroRNAs in the Pathogenesis, Prognostication and Prediction of Treatment Resistance in Soft Tissue Sarcomas.Cancers · 2023Review
- SMYD Family Members Serve as Potential Prognostic Markers and Correlate with Immune Infiltrates in Gastric Cancer.Journal of oncology · 2023Article
- The Multiple Roles of Glucose-6-Phosphate Dehydrogenase in Tumorigenesis and Cancer Chemoresistance.Life (Basel, Switzerland) · 2022Review
- Recent findings in the regulation of G6PD and its role in diseases.Frontiers in pharmacology · 2022Review
- Evidence of myomiR regulation of the pentose phosphate pathway during mechanical load-induced hypertrophy.Physiological reports · 2021Article
- Ginsenoside Rb1 and Rb2 upregulate Akt/mTOR signaling-mediated muscular hypertrophy and myoblast differentiation.Journal of ginseng research · 2020Article
- Genetics, epigenetics and redox homeostasis in rhabdomyosarcoma: Emerging targets and therapeutics.Redox biology · 2019Review
- MicroRNA-410-3p upregulation suppresses proliferation, invasion and migration, and promotes apoptosis in rhabdomyosarcoma cells.Oncology letters · 2019Article
- Defective sarcomere assembly inFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Pathogenic and Therapeutic Role of H3K4 Family of Methylases and Demethylases in Cancers.Indian journal of clinical biochemistry : IJCB · 2019Review
- The Microenvironment Is a Critical Regulator of Muscle Stem Cell Activation and Proliferation.Frontiers in cell and developmental biology · 2019Review
- The oncomir face of microRNA-206: A permanent miR-206 transfection study.Experimental biology and medicine (Maywood, N.J.) · 2018Article
- The Smyd Family of Methyltransferases: Role in Cardiac and Skeletal Muscle Physiology and Pathology.Current opinion in physiology · 2018Article
- Black ginseng activates Akt signaling, thereby enhancing myoblast differentiation and myotube growth.Journal of ginseng research · 2018Article
- Data mining and pathway analysis of glucose-6-phosphate dehydrogenase with natural language processing.Molecular medicine reports · 2017Article
- Writing, erasing and reading histone lysine methylations.Experimental & molecular medicine · 2017Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rhadomyosarcoma (RMS) is the most common soft tissue sarcoma of childhood. RMS cells resemble fetal myoblasts but are unable to complete myogenic differentiation. In previous work we showed that miR-206, which is low in RMS, when induced in RMS cells promotes the resumption of differentiation by modulating more than 700 genes. To better define the pathways involved in the conversion of RMS cells into their differentiated counterpart, we focused on 2 miR-206 effectors emerged from the microarray analysis, SMYD1 and G6PD. SMYD1, one of the most highly upregulated genes, is a H3K4 histone methyltransferase. Here we show that SMYD1 silencing does not interfere with the proliferative block or with the loss anchorage independence imposed by miR-206, but severely impairs differentiation of ERMS, ARMS, and myogenic cells. Thus SMYD1 is essential for the activation of muscle genes. Conversely, among the downregulated genes, we found G6PD, the enzyme catalyzing the rate-limiting step of the pentose phosphate shunt. In this work, we confirmed that G6PD is a direct target of miR-206. Moreover, we showed that G6PD silencing in ERMS cells impairs proliferation and soft agar growth. However, G6PD overexpression does not interfere with the pro-differentiating effect of miR-206, suggesting that G6PD downmodulation contributes to - but is not an absolute requirement for - the tumor suppressive potential of miR-206. Targeting cancer metabolism may enhance differentiation. However, therapeutic inhibition of G6PD is encumbered by side effects. As an alternative, we used DCA in combination with miR-206 to increase the flux of pyruvate into the mitochondrion by reactivating PDH. DCA enhanced the inhibition of RMS cell growth induced by miR-206, and sustained it upon miR-206 de-induction. Altogether these results link miR-206 to epigenetic and metabolic reprogramming, and suggest that it may be worth combining differentiation-inducing with metabolism-directed approaches.
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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.