Long non­coding RNA GHET1 promotes osteosarcoma development and progression via Wnt/ß­catenin signaling pathway.

Osteosarcoma (OS) is known as a malignant tumor with a high mortality rate of children and adults worldwide. Long non­coding RNAs (lncRNAs) have been revealed as oncogenes or tumor suppressors that are involved in the tumorigenesis and metastasis of some types of cancer. However, the biological role of long non­coding RNA gastric carcinoma proliferation enhancing transcript 1 (lncGHET1) and its regulatory mechanism in OS progression have not been elucidated. The aim of the present study was to investigate the role of lncGHET1 in OS. The present study explored lncGHET1 expression using a reverse transcription­quantitative (RT­q)PCR assay. Furthermore, the Cell Counting Kit­8 assay, flow cytometry detection, wound healing and transwell invasion assays were performed to evaluate its biological role and the underlying mechanisms in vitro. Additionally, the effect of lncGHET1 was evaluated in vivo in a xenograft model. lncGHET1 expression was significantly upregulated in OS cell lines compared with in an osteoblastic cell line according to the RT­qPCR assay. The results of a knockdown functional experiment suggested that inhibition of lncGHET1 attenuated cell proliferation, migration, invasion and epithelial­to­mesenchymal transition, and promoted apoptosis, partly through regulating the Wnt/ß­catenin signaling pathway in OS. These findings indicated that lncGHET1 may serve an essential regulatory role in the biological processes of OS. The present study identified a novel therapeutic target for diagnosis and treatment of human OS.