
LINC01123 enhances osteosarcoma cell growth by activating the Hedgehog pathway via the miR‐516b‐5p/Gli1 axis
Author(s) -
Pan Xiaohui,
Tan Jingxue,
Tao Tao,
Zhang Xiuwen,
Weng Yiping,
Weng Xiaokun,
Xu Jingwen,
Li Haibo,
Jiang Yuqing,
Zhou Dong,
Shen Yifei
Publication year - 2021
Publication title -
cancer science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 1347-9032
DOI - 10.1111/cas.14913
Subject(s) - gli1 , gene knockdown , cancer research , osteosarcoma , cell growth , hedgehog signaling pathway , downregulation and upregulation , oncogene , hedgehog , cell culture , cell , microrna , cell migration , metastasis , biology , microbiology and biotechnology , chemistry , signal transduction , cancer , cell cycle , gene , genetics
The lncRNA LINC01123 has been reported to act as an oncogene in many human cancers. Nevertheless, the function and underlying mechanism of LINC01123 in osteosarcoma (OS) remain unclear. This study aimed to explore the roles and mechanisms of LINC01123 in OS progression. In this study, the expression of LINC01123 was significantly upregulated in OS cell lines than in a human osteoblast cell line. Furthermore, in vitro and in vivo experiments confirmed that knockdown of LINC01123 suppressed cell progression. Mechanistically, LINC01123 acted as a competing endogenous RNA by sponging miR‐516b‐5p, thus, increasing Gli1 expression by directly targeting its 3ʹUTR. Taken together, LINC01123 enhances OS proliferation and metastasis via the miR‐516b‐5p/Gli1 axis. Therefore, LINC01123 may be a potential therapeutic target for OS treatment.