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Gene & Protein in Disease The effect of myostatin on muscle-related miRNAs

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Figure 4. Change in MSTN protein expression and proliferative characteristics in the Mstn-KO C2C12 cell line. (A) Detection of MSTN protein expression
in C2C12 monoclonal cell lines using Western blotting. (B) Evaluation of proliferative characteristics in the sgRNA1-KO, sgRNA2-KO, and CN groups
using the CCK-8 assay. (C) Representative cell cycle analysis of the sgRNA1-KO, sgRNA2-KO, and CN groups was measured using flow cytometry.
Note: **P < 0.01.

133a were significantly upregulated in both sgRNA1-KO signaling pathways, satellite cells, and other aspects are
and sgRNA2-KO groups (P < 0.01). The expression level necessary in both clinical trials and in vitro experiments to
of miR-23a was significantly upregulated (P < 0.05), better apply MSTN inhibitors in the treatment of muscle
while the expression level of miR-486 was significantly degeneration diseases.
downregulated (P < 0.05). These results indicate that Gene-knockout cell lines play an important role in the
after Mstn knockout, the transcriptional levels of multiple study of cell regulatory mechanisms. Using CRISPR/Cas9-
miRNAs were changed in C2C12 cells (Figure 5). mediated gene editing technology, Wang et al. obtained
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4. Discussion human embryonic stem cells (hESCs) with the knockout of
RelA and IκBα. Multidimensional phenotypic evaluation
Studies on the regulation and function of MSTN in both and transcriptomic analysis demonstrated that RelA
normal and pathological states, along with numerous protects vascular cells against apoptosis and regulates the
preclinical studies on the role of MSTN inhibition in mouse response of vascular inflammation to TNF-α stimulation,
models of various human diseases, have supported the providing guidance for cardiovascular disease prevention
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development of MSTN inhibitors for clinical applications. and drug development. Pascucci et al. used CRISPR/Cas9
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However, all trials on muscular dystrophy patients have technology to knock out the MAGEC2 gene in the A375
failed, mainly due to the failure of translating increased melanoma cell line, demonstrating the role of the MAGEC2
muscle mass into optimal muscle function after MSTN protein in reducing p53 transcriptional activity in cells with
inhibition, such as force ratio or fatigue resistance. overactive MEK/ERK signaling. These studies have revealed
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Changes in the function of other receptors may also the integral role played by MAGEC2 in promoting tumor
affect muscle mass or strength. In addition, inhibition development, laying the foundation for the development of
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of signaling in other cell types, such as those affecting fat anti-tumor drugs. In this study, we successfully established
content and metabolism, may interfere with muscle and stably maintained an Mstn-KO C2C12 cell line, which
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function. Due to these reasons, comprehensive studies exhibited abolished MSTN expression and enhanced cell
on Mstn gene receptors, target genes, interaction factors, growth ability. Notably, there was a significant difference
Volume 3 Issue 2 (2024) 7 doi: 10.36922/gpd.2991