Next Article in Journal
Transforming Growth Factor-Beta (TGFβ) Signaling Pathway in Cholangiocarcinoma
Next Article in Special Issue
Non-Coding RNA Regulates the Myogenesis of Skeletal Muscle Satellite Cells, Injury Repair and Diseases
Previous Article in Journal
Influenza A Hemagglutinin Passage Bias Sites and Host Specificity Mutations
Previous Article in Special Issue
MiR-501-3p Forms a Feedback Loop with FOS, MDFI, and MyoD to Regulate C2C12 Myogenesis
Open AccessArticle

PFN2a Suppresses C2C12 Myogenic Development by Inhibiting Proliferation and Promoting Apoptosis via the p53 Pathway

1
National Engineering Research Center for Breeding Swine Industry, Guangdong Provincial Key Lab of Agro-Animal Genomics and Molecular Breeding, College of Animal Science, South China Agricultural University, Guangzhou 510642, China
2
Department of Molecular Biosciences and Bioengineering, University of Hawaii at Manoa, 1955 East-West Road, Honolulu, HI 96822, USA
3
Department of Human Nutrition, Food and Animal Sciences, University of Hawaii at Manoa, 1955 East-West Road, Honolulu, HI 96822, USA
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Cells 2019, 8(9), 959; https://doi.org/10.3390/cells8090959
Received: 21 July 2019 / Revised: 17 August 2019 / Accepted: 19 August 2019 / Published: 23 August 2019
Skeletal muscle plays a crucial role in physical activity and in regulating body energy and protein balance. Myoblast proliferation, differentiation, and apoptosis are indispensable processes for myoblast myogenesis. Profilin 2a (PFN2a) is a ubiquitous actin monomer-binding protein and promotes lung cancer growth and metastasis through suppressing the nuclear localization of histone deacetylase 1 (HDAC1). However, how PFN2a regulates myoblast myogenic development is still not clear. We constructed a C2C12 mouse myoblast cell line overexpressing PFN2a. The CRISPR/Cas9 system was used to study the function of PFN2a in C2C12 myogenic development. We find that PFN2a suppresses proliferation and promotes apoptosis and consequentially downregulates C2C12 myogenic development. The suppression of PFN2a also decreases the amount of HDAC1 in the nucleus and increases the protein level of p53 during C2C12 myogenic development. Therefore, we propose that PFN2a suppresses C2C12 myogenic development via the p53 pathway. Si-p53 (siRNA-p53) reverses the PFN2a inhibitory effect on C2C12 proliferation and the PFN2a promotion effect on C2C12 apoptosis, and then attenuates the suppression of PFN2a on myogenic differentiation. Our results expand understanding of PFN2a regulatory mechanisms in myogenic development and suggest potential therapeutic targets for muscle atrophy-related diseases. View Full-Text
Keywords: proliferation; myogenic development; skeletal muscle; apoptosis; HDAC1 proliferation; myogenic development; skeletal muscle; apoptosis; HDAC1
Show Figures

Graphical abstract

MDPI and ACS Style

Li, H.; Hou, L.; Zhang, Y.; Jiang, F.; Zhu, Y.; Li, Q.X.; Hu, C.Y.; Wang, C. PFN2a Suppresses C2C12 Myogenic Development by Inhibiting Proliferation and Promoting Apoptosis via the p53 Pathway. Cells 2019, 8, 959.

Show more citation formats Show less citations formats
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop