Open Access

ARTICLE

MicroRNA-107 Promotes Proliferation, Migration, and Invasion of Osteosarcoma Cells by Targeting Tropomyosin 1

Rui Jiang^*, Chao Zhang^†, Guangyao Liu^*, Rui Gu^*, Han Wu^*

* Department of Orthopedics, China–Japan Union Hospital of Jilin University, Changchun, Jilin, P.R. China
† Department of Ophthalmology, The Second Hospital of Jilin University, Changchun, Jilin, P.R. China

Oncology Research 2017, 25(8), 1409-1419. https://doi.org/10.3727/096504017X14882829077237

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.

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