LINC01354 Promotes Osteosarcoma Cell Invasion by Up-regulating Integrin β1

Abstract

Background and aims: Long noncoding RNAs have been proved to play a key role in the development and progression of various tumors, including osteosarcoma (OS). However, the role and molecular mechanism of lncRNA in osteosarcoma metastasis remains unknown. Our purpose is to explore the clinical significance and biological function of LINC01354 in osteosarcoma.

Methods: Expression of LINC01354 in OS tissues, serum and cell lines was measured and the association between LINC01354 expression and clinicopathological factors was analyzed. The functional effects of LINC01354 were examined in vitro by using transwell assays, western blot, immunohistochemistry (IHC) and in vivo in a xenograft tumor mouse model.

Results: LINC01354 was overexpressed in OS tissues, serum and cells. LINC01354 overexpression promoted OS cells invasion, EMT and integrin β1 expression, while knockdown of LINC01354 inhibited OS cell invasion, epithelial-mesenchymal transition (EMT) and integrin β1 expression. In addition, integrin-β1 blockage with MAB13 antibody abrogated the effects of LINC01354 overexpression on promoting OS cells invasion and EMT. In addition, LINC01354 promoted OS cell metastasis in vivo.

Conclusion: LINC01354 promote OS cell EMT and invasion through up-regulating integrin β1. Our study suggested that LINC01354 may be regarded as a potential target for the clinical treatment of OS.

Keywords: EMT; Integrin β1; Invasion; LincRNA; Osteosarcoma.