MicroRNA-101 has a suppressive role in osteosarcoma cells through the targeting of c-FOS
Author(s) -
Zili Wang,
Rongzhen He,
Hansong Xia,
YU WEI,
Song Wu
Publication year - 2016
Publication title -
experimental and therapeutic medicine
Language(s) - English
Resource type - Journals
eISSN - 1792-1015
pISSN - 1792-0981
DOI - 10.3892/etm.2016.3085
Subject(s) - microrna , gene knockdown , osteosarcoma , oncogene , cell growth , cell cycle , downregulation and upregulation , cancer research , cell culture , cell , biology , apoptosis , microbiology and biotechnology , chemistry , gene , biochemistry , genetics
MicroRNAs (miRs) have been implicated in the development and progression of osteosarcoma (OS). However, the underlying mechanism of miR-101 in regulating of the proliferation, migration and invasion of OS cells remains to be elucidated. In the present study, reverse transcription-quantitative polymerase chain reaction data revealed that miR-101 was frequently downregulated in the tissue samples of 12 patients with OS compared with their matched adjacent non-tumor tissues. Furthermore, miR-101 was significantly downregulated in three common OS cell lines, Saos-2, MG63 and U2OS, compared with the human osteoblast cell line, hFOB1.19 (P<0.01). A luciferase reporter assay was also performed and identified c-FOS as a novel target of miR-101 in U2OS cells; overexpression of miR-101 significantly suppressed the protein expression levels of c-FOS, while knockdown of miR-101 significantly enhanced the formers' expression levels in U2OS cells (P<0.01). Independent inhibition of c-FOS and overexpression of miR-101 expression levels significantly suppressed U2OS cell proliferation, migration and invasion (P<0.01). However, overexpression of c-FOS reversed the inhibitory effect of miR-101 upregulation on proliferation, migration and invasion of U2OS cells, suggesting that miR-101 acts as a tumor suppressor in OS cells via targeting of c-FOS. Thus, we propose that the miR-101/c-FOS axis may be a potential therapeutic target for OS.
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