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miR‐16 inhibits cell proliferation by targeting IGF1R and the Raf1–MEK1/2–ERK1/2 pathway in osteosarcoma
Author(s) -
Chen Lei,
Wang Qing,
Wang Guo-dong,
Wang Hua-song,
Huang Yong,
Liu Xi-ming,
Cai Xian-hua
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.03.007
Subject(s) - insulin like growth factor 1 receptor , osteosarcoma , cell growth , cancer research , microrna , suppressor , cell , microbiology and biotechnology , biology , cancer , gene , receptor , growth factor , genetics
Several miRNAs have been implicated in the development and progression of osteosarcoma (OS). In this study, we found that miR‐16 is downregulated in OS cell lines and tissues. Overexpression of miR‐16 suppresses OS cell proliferation and tumor growth in nude mice. Furthermore, we confirmed that IGF1R is a direct target of miR‐16. Mechanistic investigation revealed that miR‐16 overexpression inhibits the Raf1–MEK1/2–ERK1/2 pathway. In clinical specimens, IGF1R levels inversely correlate with miR‐16 expression. Our results provide significant clues regarding the role of miR‐16 as a tumor suppressor by targeting IGF1R in OS.