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TBRG4 敲低通过 PI3K/Akt 信号通路抑制人骨肉瘤细胞系 MG63 的增殖和生长
Authors Huang F, Liao F, Ma G, Hu Y, Zhang C, Xu P, Xu T, Chang J
Received 12 February 2020
Accepted for publication 14 May 2020
Published 27 July 2020 Volume 2020:13 Pages 7271—7281
DOI https://doi.org/10.2147/OTT.S249477
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Carlos E Vigil
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: TBRG4, osteosarcoma, proliferation, PI3K/Akt, MG63 cells
