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MiR-100 Inhibits Osteosarcoma Cell Proliferation, Migration, and Invasion and Enhances Chemosensitivity by Targeting IGFIR
Author(s) -
Yang Liu,
Shutao Zhu,
Xiao Wang,
Jun Deng,
Weihua Li,
Peng Zhang,
Bingshan Liu
Publication year - 2015
Publication title -
technology in cancer research and treatment
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.754
H-Index - 63
eISSN - 1533-0346
pISSN - 1533-0338
DOI - 10.1177/1533034615601281
Subject(s) - osteosarcoma , microrna , cancer research , cell growth , mapk/erk pathway , biology , pi3k/akt/mtor pathway , protein kinase b , cell , cell migration , growth factor , receptor , signal transduction , microbiology and biotechnology , gene , genetics
MicroRNAs are highly conserved noncoding RNA that negatively modulate protein expression at a posttranscriptional and/or translational level. MicroRNAs play an important role in the development and progression of human cancers, including osteosarcoma. Recent studies have shown that miR-100 was downregulated in many cancers; however, the role of miR-100 in human osteosarcoma has not been totally elucidated. In this study, we demonstrate that the expression of miR-100 was significantly downregulated in human osteosarcoma tissues compared to the adjacent tissues. Enforced expression of miR-100 inhibited cell proliferation, migration, and invasion abilities of osteosarcoma cells, U-2OS, and MG-63. Additionally, miR-100 also sensitized osteosarcoma cells to cisplatin and promoted apoptosis. Furthermore, overexpression of miR-100 decreased the expression of insulin-like growth factor I receptor and inhibited PI3K/AKT and MAPK/ERK signaling. In human clinical specimens, insulin-like growth factor I receptor was inversely correlated with miR-100 in osteosarcoma tissues. Collectively, our results demonstrate that miR-100 is a tumor suppressor microRNA and indicate its potential application for the treatment of osteosarcoma in future.

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