Long noncoding RNA SAM promotes myoblast proliferation through stabilizing Sugt1 and facilitating kinetochore assembly

Li, Yuying; Yuan, Jie; Chen, Fengyuan; Zhang, Suyang; Zhao, Yu; Chen, Xiaona; Lu, Leina; Zhou, Liang; Chu, Ching-Chi; Sun, Hao; Wang, Huating

doi:10.1038/s41467-020-16553-6

Cited by 28 publications

(36 citation statements)

References 56 publications

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“…Recently, Li et al found that the lncRNA MSTRG.42019 was associated with skeletal muscle fiber-type switching in pigs [ 53 ]. Several lncRNAs, such as LncMyoD , SAM , H19 , and CTTN-IT1 , affect the activity of satellite cells in mice, pigs, and sheep [ 54 , 55 , 56 , 57 ]. The in vivo silencing of Pvt1 results in increases in the size and number of mitochondria [ 20 ].…”

Section: Discussionmentioning

confidence: 99%

An Analysis of Differentially Expressed Coding and Long Non-Coding RNAs in Multiple Models of Skeletal Muscle Atrophy

Hitachi

Nakatani

Kiyofuji

et al. 2021

IJMS

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The loss of skeletal muscle mass (muscle atrophy or wasting) caused by aging, diseases, and injury decreases quality of life, survival rates, and healthy life expectancy in humans. Although long non-coding RNAs (lncRNAs) have been implicated in skeletal muscle formation and differentiation, their precise roles in muscle atrophy remain unclear. In this study, we used RNA-sequencing (RNA-Seq) to examine changes in the expression of lncRNAs in four muscle atrophy conditions (denervation, casting, fasting, and cancer cachexia) in mice. We successfully identified 33 annotated lncRNAs and 18 novel lncRNAs with common expression changes in all four muscle atrophy conditions. Furthermore, an analysis of lncRNA–mRNA correlations revealed that several lncRNAs affected small molecule biosynthetic processes during muscle atrophy. These results provide novel insights into the lncRNA-mediated regulatory mechanism underlying muscle atrophy and may be useful for the identification of promising therapeutic targets.

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Section: Discussionmentioning

confidence: 99%

An Analysis of Differentially Expressed Coding and Long Non-Coding RNAs in Multiple Models of Skeletal Muscle Atrophy

Hitachi

Nakatani

Kiyofuji

et al. 2021

IJMS

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“…Skeletal muscle development is tightly regulated by a complex network. Increasing evidence indicates that lncRNAs may play a crucial role in regulating myogenesis ( Ballarino et al, 2018 ; Jin et al, 2018 ; Militello et al, 2018 ; Zhang et al, 2018c ; Li et al, 2019 , 2020 ; Sui et al, 2019 ). In the present study, the biological function of a novel lncRNA, lnc-GD2H, in regulating myoblast proliferation and differentiation and muscle regeneration was determined ( Figure 9 ).…”

Section: Discussionmentioning

confidence: 99%

Lnc-GD2H Promotes Proliferation by Forming a Feedback Loop With c-Myc and Enhances Differentiation Through Interacting With NACA to Upregulate Myog in C2C12 Myoblasts

Chen

Liu

She

et al. 2021

Front. Cell Dev. Biol.

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In the present study, the roles of a novel long non-coding RNA (lncRNA), lnc-GD2H, in promoting C2C12 myoblast proliferation and differentiation and muscle regeneration were investigated by quantitative polymerase chain reaction, western blotting, Cell Counting Kit-8, 5-ethynyl-2′-deoxyuridine (EdU), immunofluorescence staining, luciferase reporter, mass spectrometry, pulldown, chromatin immunoprecipitation, RNA immunoprecipitation assay, wound healing assays, and cardiotoxin (CTX)-induced muscle injury assays. It was observed that lnc-GD2H promoted myoblast proliferation as evidenced by the enhancement of the proliferation markers c-Myc, CDK2, CDK4, and CDK6, percentage of EdU-positive cells, and rate of cell survival during C2C12 myoblast proliferation. Additional experiments confirmed that c-Myc bound to the lnc-GD2H promoter and regulated its transcription. lnc-GD2H promoted cell differentiation with enhanced MyHC immunostaining as well as increased expression of the myogenic marker genes myogenin (Myog), Mef2a, and Mef2c during myoblast differentiation. Additional assays indicated that lnc-GD2H interacted with NACA which plays a role of transcriptional regulation in myoblast differentiation, and the enrichment of NACA at the Myog promoter was impaired by lnc-GD2H. Furthermore, inhibition of lnc-GD2H impaired muscle regeneration after CTX-induced injury in mice. lnc-GD2H facilitated the expression of proliferating marker genes and formed a feedback loop with c-Myc during myoblast proliferation. In differentiating myoblasts, lnc-GD2H interacted with NACA to relieve the inhibitory effect of NACA on Myog, facilitating Myog expression to promote differentiation. The results provide evidence for the role of lncRNAs in muscle regeneration and are useful for developing novel therapeutic targets for muscle disorders.

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“…To induce myogenic differentiation, fetal bovine serum was replaced by horse serum (2%, final concentration, Gibco) in culture medium. Mouse satellite cells were isolated and cultured as described before ( Li et al, 2020 ). Cells were maintained in a humidified incubator at 37°C and 5% CO 2 atmosphere.…”

Section: Methodsmentioning

confidence: 99%

miR-130b inhibits proliferation and promotes differentiation in myocytes via targeting Sp1

Wang

Yao

et al. 2021

Journal of Molecular Cell Biology

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Muscle regeneration after damage or during myopathies requires a fine cooperation between myoblast proliferation and myogenic differentiation. A growing body of evidence suggests that microRNAs play critical roles in myocyte proliferation and differentiation transcriptionally. However, the molecular mechanisms underlying the orchestration are not fully understood. Here, we showed that miR-130b is able to repress myoblast proliferation and promote myogenic differentiation via targeting Sp1 transcription factor. Importantly, overexpression of miR-130b is capable of improving the recovery of damaged muscle in a freeze injury model. Moreover, miR-130b expression is declined in the muscle of muscular dystrophy patients. Thus, these results indicated that miR-130b may play a role in skeletal muscle regeneration and myopathy progression. Together, our findings suggest that the miR-130b/Sp1 axis may serve as a potential therapeutic target for the treatment of patients with muscle damage or severe myopathies.

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Long noncoding RNA SAM promotes myoblast proliferation through stabilizing Sugt1 and facilitating kinetochore assembly

Cited by 28 publications

References 56 publications

An Analysis of Differentially Expressed Coding and Long Non-Coding RNAs in Multiple Models of Skeletal Muscle Atrophy

An Analysis of Differentially Expressed Coding and Long Non-Coding RNAs in Multiple Models of Skeletal Muscle Atrophy

Lnc-GD2H Promotes Proliferation by Forming a Feedback Loop With c-Myc and Enhances Differentiation Through Interacting With NACA to Upregulate Myog in C2C12 Myoblasts

miR-130b inhibits proliferation and promotes differentiation in myocytes via targeting Sp1

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