The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs
Myostatin (MSTN) is a member of the TGF-β superfamily that negatively regulates skeletal muscle growth and differentiation. However, the mechanism by which complete MSTN deletion limits excessive proliferation of muscle cells remains unclear. In this study, we knocked out MSTN in mouse myob...
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2019-02-01
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| Series: | International Journal of Molecular Sciences |
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| author | Peixuan Huang Daxin Pang Kankan Wang Aishi Xu Chaogang Yao Mengjing Li Wenni You Qiushuang Wang Hao Yu |
| author_facet | Peixuan Huang Daxin Pang Kankan Wang Aishi Xu Chaogang Yao Mengjing Li Wenni You Qiushuang Wang Hao Yu |
| author_sort | Peixuan Huang |
| collection | DOAJ |
| description | Myostatin (MSTN) is a member of the TGF-β superfamily that negatively regulates skeletal muscle growth and differentiation. However, the mechanism by which complete MSTN deletion limits excessive proliferation of muscle cells remains unclear. In this study, we knocked out MSTN in mouse myoblast lines using a Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR/Cas9) system and sequenced the mRNA and miRNA transcriptomes. The results show that complete loss of MSTN upregulates seven miRNAs targeting an interaction network composed of 28 downregulated genes, including <i>TGFB1</i>, <i>FOS</i> and <i>RB1</i>. These genes are closely associated with tumorigenesis and cell proliferation. Our study suggests that complete loss of MSTN may limit excessive cell proliferation via activation of miRNAs. These data will contribute to the treatment of rhabdomyosarcoma (RMS). |
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| spelling | doaj.art-5a152443f5bb4258abf9637cfe2caf1d2022-12-22T03:50:38ZengMDPI AGInternational Journal of Molecular Sciences1422-00672019-02-0120364310.3390/ijms20030643ijms20030643The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAsPeixuan Huang0Daxin Pang1Kankan Wang2Aishi Xu3Chaogang Yao4Mengjing Li5Wenni You6Qiushuang Wang7Hao Yu8Jilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, ChinaJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, ChinaJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, ChinaJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, ChinaJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, ChinaJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, ChinaJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, ChinaPublic Computer Education and Research Center, Jilin University, Changchun 130062, ChinaJilin Provincial Key Laboratory of Animal Embryo Engineering, College of Animal Sciences, Jilin University, Changchun 130062, ChinaMyostatin (MSTN) is a member of the TGF-β superfamily that negatively regulates skeletal muscle growth and differentiation. However, the mechanism by which complete MSTN deletion limits excessive proliferation of muscle cells remains unclear. In this study, we knocked out MSTN in mouse myoblast lines using a Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR/Cas9) system and sequenced the mRNA and miRNA transcriptomes. The results show that complete loss of MSTN upregulates seven miRNAs targeting an interaction network composed of 28 downregulated genes, including <i>TGFB1</i>, <i>FOS</i> and <i>RB1</i>. These genes are closely associated with tumorigenesis and cell proliferation. Our study suggests that complete loss of MSTN may limit excessive cell proliferation via activation of miRNAs. These data will contribute to the treatment of rhabdomyosarcoma (RMS).https://www.mdpi.com/1422-0067/20/3/643MSTNRNA-seqmiRNA-seqtranscriptomicsC2C12RMS |
| spellingShingle | Peixuan Huang Daxin Pang Kankan Wang Aishi Xu Chaogang Yao Mengjing Li Wenni You Qiushuang Wang Hao Yu The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs International Journal of Molecular Sciences MSTN RNA-seq miRNA-seq transcriptomics C2C12 RMS |
| title | The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs |
| title_full | The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs |
| title_fullStr | The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs |
| title_full_unstemmed | The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs |
| title_short | The Possible Role of Complete Loss of Myostatin in Limiting Excessive Proliferation of Muscle Cells (C2C12) via Activation of MicroRNAs |
| title_sort | possible role of complete loss of myostatin in limiting excessive proliferation of muscle cells c2c12 via activation of micrornas |
| topic | MSTN RNA-seq miRNA-seq transcriptomics C2C12 RMS |
| url | https://www.mdpi.com/1422-0067/20/3/643 |
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