TBRG4 Knockdown Suppresses Proliferation and Growth of Human Osteosarcoma Cell Lines MG63 Through PI3K/Akt Pathway

Fei Huang; Faxue Liao; Guangwen Ma; Yong Hu; Chi Zhang; Pengfei Xu; Tangbing Xu; Jun Chang

doi:10.2147/OTT.S249477

TBRG4 Knockdown Suppresses Proliferation and Growth of Human Osteosarcoma Cell Lines MG63 Through PI3K/Akt Pathway

Onco Targets Ther. 2020 Jul 27:13:7271-7281. doi: 10.2147/OTT.S249477. eCollection 2020.

Authors

Fei Huang^#¹, Faxue Liao^#¹, Guangwen Ma¹, Yong Hu², Chi Zhang¹, Pengfei Xu¹, Tangbing Xu¹, Jun Chang³

Affiliations

¹ Department of Orthopaedics, The Fourth Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China.
² Department of Orthopaedics, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China.
³ Clinical Research Centre, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.

^# Contributed equally.

Abstract

Background: The transforming growth factor β regulator 4 (TBRG4) has been proved to be involved in various types of tumor. However, its contribution in human osteosarcoma (OS) is still unclear.

Patients and methods: In the present study, immunohistochemistry and quantitative real-time PCR were performed to investigate the expression of TBRG4 in OS tissues obtained from patients and three types of cell lines. The effect of TBRG4 knockdown using lentivirus on tumorigenesis was detected by CCK8, high-content screening analysis, colony formation assay and flow cytometric analysis. Bioinformatics analysis was operated to investigate related signaling pathways following TBRG4 knockdown.

Results: The results showed that the expression of TBRG4 increased significantly in OS tissues and MG63 cell line. TBRG4 knockdown inhibited cell proliferation, colony and tumor formation, while activating cell apoptosis. Ingenuity Pathway Analysis and Western blot assay further indicated that TBRG4 knockdown may regulate the proliferation of human MG63 cells through PI3K/Akt signaling pathway.

Conclusion: Our results suggest that TBRG4 may become a promising therapeutic target for the treatment of human OS.

Keywords: MG63 cells; PI3K/Akt; TBRG4; osteosarcoma; proliferation.

Grants and funding

This project was supported by the Postdoctoral Science Foundation of China (No. 2019M662994) and the Natural Science Foundation of China (No. 81601974).