Long non-coding RNA ERVK13-1 aggravates osteosarcoma through the involvement of microRNA-873-5p/KLF5 axis

  • Han Xie 1Department of Orthopedics, Guangzhou Red Cross Hospital Affiliated to Jinan University, Guangzhou, Guangdong 510000, P.R. China; 2Department of Orthopedics, Huizhou Central People’s Hospital, Huizhou, Guangdong 516000, P.R. China
  • Libing Dai Department of Orthopedics, Guangzhou Red Cross Hospital Affiliated to Jinan University, Guangzhou, Guangdong 510000, P.R. China
  • Baoqing Ye Department of Orthopedics, Guangzhou Red Cross Hospital Affiliated to Jinan University, Guangzhou, Guangdong 510000, P.R. China
  • Ruixiong Chen Department of Orthopedics, Huizhou Central People’s Hospital, Huizhou, Guangdong 516000, P.R. China
  • Bin Wang Department of Orthopedics, Huizhou First Hospital, Huizhou, Guangdong 516000, P.R. China
  • Nanwei Zhang Department of Orthopedics, Huizhou Central People’s Hospital, Huizhou, Guangdong 516000, P.R. China
  • Haixiong Miao Department of Orthopedics, Guangzhou Red Cross Hospital Affiliated to Jinan University, Guangzhou, Guangdong 510000, P.R. China
  • Weiguo Liang Department of Orthopedics, Guangzhou Red Cross Hospital Affiliated to Jinan University, Guangzhou, Guangdong 510000, P.R. China
DOI: https://doi.org/10.18388/abp.2020_5809

Abstract

Objective: To explore the effect and mechanism of long noncoding RNA ERVK13-1 on osteosarcoma (OS) cell development by regulation of miR-873-5p/KLF5 axis. Methods: The expression of ERVK13-1 in the collected tissue was detected by RT-qPCR, and then the relationship between ERVK13-1 expression and clinical characteristics of OS patients was analyzed. After OS cell lines were transfected with miR-873-5p inhibitor, si-ERVK13-1, si-KLF5 or their negative controls, the expression of ERVK13-1, miR-873-5p, and KLF5 in OS cell lines were measured, followed by determination of their effects on cell proliferation, migration, and invasion abilities. Moreover, the binding relationships of ERVK13-1 and miR-873-5p, as well as miR-873-5p and KLF5, were verified by the dual-luciferase reporter gene assay. Results: Highly expressed ERVK13-1 was found in OS tissues, which was closely related to tumor size, tumor node metastasis, and distant metastasis. The overall survival of OS patients with high expression of ERVK13-1 was poorer than those with low expression of ERVK13-1. Elevated ERVK13-1 and KLF5 but suppressed miR-873-5p was observed in the OS cell lines U2OS and MG63. Transfection with miR-873-5p inhibitor enhanced the malignant potentials of OS cells, and transfection with si-ERVK13-1 or si-KLF5 reduced these abilities of OS cells. ERVK13-1 bound to miR-873-5p and KLF5 was a target gene of miR-873-5p. Conclusion: The ERVK13-1/miR-873-5p/KLF5 axis confers vital effect on the occurrence and progression of OS, thus providing possible guidance for the clinical treatment of OS.

Published
2022-10-22
Issue
Vol. 69 No. 4 (2022)
Section
Articles

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