OncoTargets and Therapy (Jul 2020)

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

  • Huang F,
  • Liao F,
  • Ma G,
  • Hu Y,
  • Zhang C,
  • Xu P,
  • Xu T,
  • Chang J

Journal volume & issue
Vol. Volume 13
pp. 7271 – 7281

Abstract

Read online

Fei Huang,1,* Faxue Liao,1,* Guangwen Ma,1 Yong Hu,2 Chi Zhang,1 Pengfei Xu,1 Tangbing Xu,1 Jun Chang3 1Department of Orthopaedics, The Fourth Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People’s Republic of China; 2Department of Orthopaedics, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People’s Republic of China; 3Clinical Research Centre, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jun ChangClinical Research Centre, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong, People’s Republic of ChinaTel/ Fax + 86 551 66331115Email [email protected]: 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: TBRG4, osteosarcoma, proliferation, PI3K/Akt, MG63 cells

Keywords