z-logo
open-access-imgOpen Access
Long non‑coding RNA GHET1 promotes osteosarcoma development and progression via Wnt/β‑catenin signaling pathway
Author(s) -
Xingli Chen,
Wei Zhao,
Weimin Fan
Publication year - 2020
Publication title -
oncology reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.094
H-Index - 96
eISSN - 1791-2431
pISSN - 1021-335X
DOI - 10.3892/or.2020.7585
Subject(s) - wnt signaling pathway , cancer research , gene knockdown , cell cycle , carcinogenesis , long non coding rna , oncogene , cell growth , biology , osteosarcoma , epithelial–mesenchymal transition , tumor progression , flow cytometry , cell , metastasis , cancer , apoptosis , signal transduction , downregulation and upregulation , microbiology and biotechnology , gene , genetics
Osteosarcoma (OS) is known as a malignant tumor with a high mortality rate of children and adults worldwide. Long non‑coding 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 non‑coding 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 transcription‑quantitative (RT‑q)PCR assay. Furthermore, the Cell Counting Kit‑8 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 RT‑qPCR assay. The results of a knockdown functional experiment suggested that inhibition of lncGHET1 attenuated cell proliferation, migration, invasion and epithelial‑to‑mesenchymal transition, and promoted apoptosis, partly through regulating the Wnt/β‑catenin 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.

The content you want is available to Zendy users.

Already have an account? Click here to sign in.
Having issues? You can contact us here
Accelerating Research

Address

John Eccles House
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom