@Article{096504017X14882829077237,
AUTHOR = {Rui Jiang, Chao Zhang, Guangyao Liu, Rui Gu, Han Wu},
TITLE = {MicroRNA-107 Promotes Proliferation, Migration, and Invasion of  Osteosarcoma Cells by Targeting Tropomyosin 1},
JOURNAL = {Oncology Research},
VOLUME = {25},
YEAR = {2017},
NUMBER = {8},
PAGES = {1409--1419},
URL = {http://www.techscience.com/or/v25n8/56926},
ISSN = {1555-3906},
ABSTRACT = {Osteosarcoma is the most common primary bone malignancy manifested predominantly in children and young 
adults. Studies indicate that miR-107 is involved in the pathogenesis of osteosarcoma and that tropomyosin 1 
(TPM1) acts as a tumor suppressor in many types of cancer. In this study, we analyzed the effect of miR-107 on 
human osteosarcoma cells and investigated the mechanism in which TPM1 is involved. miR-107 expression in 
human osteosarcoma tissues and cells was analyzed in quantitative real-time PCR (qRT-PCR). Human osteosarcoma (U2OS) cells were transfected with miR-107 mimic, inhibitor, or scramble controls to evaluate the effect 
of miR-107 on cellular migration and invasion, cell viability, and apoptosis. Cells were cotransfected with the 
miR-107 mimic and TPM1 3'-UTR wild-type (wt) recombinant vector or mutant type (mt) as a negative control. 
The binding effect of miR-107 on TPM1 3'-UTR was determined by dual-luciferase reporter assay. The expression of TPM1, apoptosis-related proteins, and signaling molecules was determined by qRT-PCR and Western 
blotting. The results showed that miR-107 expression was upregulated in osteosarcoma tissues and cell lines. 
miR-107 overexpression promoted U2OS cell viability, migration, and invasion whereas it inhibited apoptosis. 
miR-107 inhibitor transfection ameliorated or abolished these effects after miR-107 binding to TPM1 3'-UTR-wt 
regulated TPM1 expression. miR-107 in U2OS cells activated MEK/ERK and NF-kB signaling pathways via 
TPM1. In conclusion, miR-107 overexpression promoted U2OS cell viability, migration, and invasion via downregulation of TPM1 and might be through activating the MEK/ERK and NF-kB signaling pathways.},
DOI = {10.3727/096504017X14882829077237}
}