PMID- 32652105 OWN - NLM STAT- MEDLINE DCOM- 20200826 LR - 20211204 IS - 1879-0038 (Electronic) IS - 0378-1119 (Linking) VI - 757 DP - 2020 Oct 5 TI - Overexpression of the Tuberous sclerosis complex 2 (TSC2) gene inhibits goat myoblasts proliferation and differentiation in understanding the underlying mechanism of muscle development. PG - 144943 LID - S0378-1119(20)30612-0 [pii] LID - 10.1016/j.gene.2020.144943 [doi] AB - The growth of animal skeletal muscle is mainly determined by the synthesis processes of total proteins in skeletal muscle cells, which has a significant impact on the postnatal growth of young animals. An increasing number of studies are focusing on the functions of Tuberous sclerosis complex 2 (TSC2) during the process of cell protein synthesis and growth. However, it is still unclear the effect of whether and how TSC2 on goat myoblasts proliferation and differentiation. Here, we found that TSC2 gene has opposite expression patterns in proliferation and differentiation of myoblasts. An expression vector containing goat TSC2 cDNA sequences linked with pcDNA3.1 plasmid was constructed. Myoblasts proliferation activity was significantly inhibited and cell cycle transition slowed down after the transfection of pcDNA3.1-TSC2 plasmid into goat primary myoblasts by EdU staining, CCK-8 and flow cytometry. Mechanically, we further confirmed that the overexpression TSC2 was able to down-regulate the mRNA and protein expression of mechanistic target of rapamycin (mTOR), p70 ribosomal S6 kinase 1 (p70S6K) and some cell cycle related genes. In addition, the expression of myogenic genes and myotube formation were attenuated. Collectively, all our results of the experiment demonstrate that TSC2 could regulate myoblasts cells proliferation and differentiation via the activation of the mTOR/p70S6K signaling pathway. CI - Copyright (c) 2020 Elsevier B.V. All rights reserved. FAU - Lyu, Ming AU - Lyu M AD - Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, China. FAU - Shalitana, Alai AU - Shalitana A AD - Department of Xinjiang Institute for Cancer Research, Xinjiang Cancer Hospital of Xinjiang Medical University, Urumqi 830011, China. FAU - Luo, Jun AU - Luo J AD - Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, China. FAU - He, Huanshan AU - He H AD - Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, China. FAU - Sun, Shuang AU - Sun S AD - Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, China. FAU - Wang, Ping AU - Wang P AD - Key Laboratory of Animal Genetics, Breeding and Reproduction of Shaanxi Province, College of Animal Science and Technology, Northwest A&F University, Yangling, Shaanxi 712100, China. Electronic address: wangping@nwafu.edu.cn. LA - eng PT - Journal Article DEP - 20200709 PL - Netherlands TA - Gene JT - Gene JID - 7706761 RN - 0 (Cell Cycle Proteins) RN - 0 (Tuberous Sclerosis Complex 2 Protein) RN - EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 70-kDa) RN - EC 2.7.11.1 (TOR Serine-Threonine Kinases) SB - IM MH - Animals MH - Cell Cycle Proteins/genetics/metabolism MH - *Cell Differentiation MH - *Cell Proliferation MH - Cells, Cultured MH - Goats MH - *Muscle Development MH - Myoblasts/cytology/*metabolism/physiology MH - Ribosomal Protein S6 Kinases, 70-kDa/genetics/metabolism MH - TOR Serine-Threonine Kinases/genetics/metabolism MH - Tuberous Sclerosis Complex 2 Protein/*genetics/metabolism MH - Up-Regulation OTO - NOTNLM OT - Differentiation OT - Goat myoblasts OT - MTOR/p70S6K OT - Proliferation OT - TSC2 COIS- Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper. EDAT- 2020/07/12 06:00 MHDA- 2020/08/28 06:00 CRDT- 2020/07/12 06:00 PHST- 2019/10/27 00:00 [received] PHST- 2020/06/26 00:00 [revised] PHST- 2020/07/01 00:00 [accepted] PHST- 2020/07/12 06:00 [pubmed] PHST- 2020/08/28 06:00 [medline] PHST- 2020/07/12 06:00 [entrez] AID - S0378-1119(20)30612-0 [pii] AID - 10.1016/j.gene.2020.144943 [doi] PST - ppublish SO - Gene. 2020 Oct 5;757:144943. doi: 10.1016/j.gene.2020.144943. Epub 2020 Jul 9.