Forkhead box C1 is targeted by microRNA‑133b and promotes cell proliferation and migration in osteosarcoma
Affiliations: Mental Health Institute, Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, P.R. China, Department of Orthopedics, Second Xiangya Hospital of Central South University, Changsha, Hunan 410011, P.R. China
- Published online on: August 2, 2017 https://doi.org/10.3892/etm.2017.4870
- Pages: 2823-2830
Copyright: © Deng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
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Forkhead box C1 (FOXC1) has been demonstrated to act as an oncogene in a number of malignant tumors, though its underlying mechanism of action in osteosarcoma (OS) remains unknown. The present study evaluated the expression and regulatory role of FOXC1 in OS. Reverse transcription‑quantitative polymerase chain reaction and western blot data indicated that FOXC1 was significantly upregulated in OS tissues and cell lines when compared with adjacent non‑tumor tissues (P<0.001) and normal human osteoblast cells (P<0.01), respectively. Moreover, levels of FOXC1 expression were significantly higher in OS at advanced clinical stage (III‑IV) when compared with that at low clinical stage (I‑II; P<0.001). Knockdown of FOXC1 expression caused a significant decrease in the proliferation and migration of OS U2OS cells (P<0.01), while overexpression of FOXC1 significantly promoted U2OS cell proliferation and migration (P<0.01), relative to control U2OS cells. Furthermore, FOXC1 was identified as a direct target of microRNA (miR)‑133b, a reported tumor‑suppressive miR in OS. The protein expression of FOXC1 was negatively regulated by miR‑133b in U2OS cells (P<0.01), and miR‑133b expression was inversely correlated with FOXC1 expression in OS. In conclusion, the present study demonstrated that FOXC1, targeted by miR‑133b, may promote cell proliferation and migration in OS. Thus, FOXC1 may be a potential therapeutic target in the treatment of OS.