J Cancer 2019; 10(8):1855-1861. doi:10.7150/jca.28476 This issue

Research Paper

BTF3 Silencing Inhibits the Proliferation of Osteosarcoma Cells

Qi Liu1, Lin Jiang2, Wanchun Wang3, Tao Jiang 3✉

1. Department of General Surgery, People's Hospital of Hunan Province, First Affiliated Hospital of Hunan Normal University, Changsha 410005, Hunan Province, China
2. Department of Orthopedic Surgery, Traumatology and Orthopedics Hospital of Liuyang, Liuyang 410300, Hunan Province, China
3. Department of Orthopedic Surgery, The Second Xiangya Hospital, Central South University, Changsha 410005, Hunan Province, China

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Citation:
Liu Q, Jiang L, Wang W, Jiang T. BTF3 Silencing Inhibits the Proliferation of Osteosarcoma Cells. J Cancer 2019; 10(8):1855-1861. doi:10.7150/jca.28476. Available from https://www.jcancer.org/v10p1855.htm

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Abstract

Osteosarcoma (OS) is one of the bone malignancy cancers with poor prognosis in the early stages worldwide. Basic transcription factor 3 (BTF3) is associated with the development of several types of cancer. The present study aimed to evaluate the role of BTF3 in OS. Silencing of BTF3 was achieved by using stable lentivirus transfection of siRNA targeting BTF3 in the human OS cell line Saos-2. Cell viability and colony-forming ability were measured using methyl-thaizolyl-tetrazolium (MTT) and colony formation assays, respectively. Propidium iodide staining and flow cytometry was used to detect the progression of the cell cycle. To evaluate the possible intracellular signaling molecules involved, a PathScan Intracellular Signaling Array Kit was utilized. Lentivirus-BTF3-shRNA (LV-BTF3-shRNA) suppressed expression of BTF3 in Saos-2 cells (inhibition ratio: 89.8%), which significantly inhibited cell proliferation (48.5%), colony formation and enhanced apoptosis to 48.2% compared to 4.5% with lentivirus control shRNA (N-shRNA). Additionally, BTF3 silencing enhanced the percentage of Saos-2 cells in S and G2/M phases, but significantly reduced cells in the G0/M phase (all P < 0.01). The proteins activated by BTF3 included STAT3, S6 ribosomal protein, HSP27 and SAPK/JNK2, all of which were inhibited by BTF3 silencing, whereas SAPK/JNK1 was upregulated by BTF3 silencing. In the present study, we explored the crucial role of BTF3 in promoting OS cell proliferation as well as laying the foundations for further research to investigate the clinical potential of lentivirus-mediated delivery of BTF3 interruption therapy for the treatment of OS.

Keywords: osteosarcoma, basic transcription factor 3, Saos-2, STAT3, S6 ribosomal protein, HSP27