ArticleEpigenetics2023
MYOD induced lnc-MEG3 promotes porcine satellite cell differentiation via interacting with DLST.
Article in Epigenetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- LncRNA MEG3 regulates the development of porcine skeletal muscle satellite cells by enhancing HMGA1 stability.Cellular & molecular biology letters · 2026Article
- LncRNA-MEG3 Regulates Muscle Mass and Metabolic Homeostasis by Facilitating SUZ12 Liquid-Liquid Phase Separation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Single-nucleus transcriptomic analysis reveals the regulatory circuitry of myofiber XBP1 during regenerative myogenesis.iScience · 2024Article
- LncRNA GTL2 regulates myoblast proliferation and differentiation via the PKA-CREB pathway in Duolang sheep.Zoological research · 2024Article
- Molecular Regulation of Porcine Skeletal Muscle Development: Insights from Research on CDC23 Expression and Function.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNAs (lncRNAs) are involved in the process of muscle cell differentiation and play an important role. Previous studies have shown that lncRNA-MEG3 promotes the differentiation of porcine skeletal muscle satellite cells (PSCs), but the regulatory mechanism of MEG3 interaction with target protein has not been well studied. We demonstrated that MEG3 can bind dihydrolipoamide succinyltransferase (DLST) by RNA pull down and RIP-qPCR. Subsequently, knockdown and overexpression experiments showed that DLST promotes PSCs differentiation. Rescue experiments showed that the expression of DLST protein was significantly increased with MEG3 overexpression and decreased with MEG3 knockdown, while its mRNA expression was not changed. Furthermore, we have successfully predicted and validated that the transcription factor myogenic differentiation (MYOD) binds to the MEG3 core promoter though utilizing chromatin immunoprecipitation (CHIP) and luciferase reporter assays. The results indicated that MYOD acts as a transcription factor of MEG3 to promote MEG3 transcription. Knockdown of MEG3 in vivo indicated that MEG3 is involved in skeletal muscle regeneration. It is concluded that MYOD acts as a transcription factor to induce MEG3 expression. MEG3 acts as a molecular scaffold to bind and promote DLST protein expression. This paper provides a new molecular mechanism for MEG3 to promote the differentiation of PSCs.
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Registered trials
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 Socratic graph.