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FOXO1–MALAT1–miR-26a-5p Feedback Loop Mediates Proliferation and Migration in Osteosarcoma Cells

Juntao Wang, Guodong Sun

Department of Traditional Chinese Orthopedics and Traumatology, the Affiliated Hospital of Shandong Academy of Medical Sciences, Jinan, Shandong Province, P.R. China

Oncology Research 2017, 25(9), 1517-1527. https://doi.org/10.3727/096504017X14859934460780

Abstract

miR-26a has been found to be downregulated in osteosarcoma (OS) when compared with normal control tissues and has been shown to suppress the malignant behaviors of OS cells. The underlying mechanism, nevertheless, remains unknown. In our study, the long noncoding RNA MALAT1, confirmed to be significantly upregulated in OS, is first shown to be capable of promoting proliferation and migration by directly suppressing miR-26a-5p in OS cells. In addition, we have identified forkhead box O1 (FOXO1) as a transcriptional factor of MALAT1 that can negatively regulate MALAT1. We have shown that MALAT1 promoted growth and migration through inhibiting miR-26a-5p in OS cells. Suppression of FOXO1, identified as a regulatory transcriptional factor of MALAT1, was shown to be able to slow down both proliferation and metastases in OS cells, suggesting that targeting FOXO1 can be useful in the therapy of patients with OS.

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APA Style
Wang, J., Sun, G. (2017). Foxo1–malat1–mir-26a-5p feedback loop mediates proliferation and migration in osteosarcoma cells. Oncology Research, 25(9), 1517-1527. https://doi.org/10.3727/096504017X14859934460780
Vancouver Style
Wang J, Sun G. Foxo1–malat1–mir-26a-5p feedback loop mediates proliferation and migration in osteosarcoma cells. Oncol Res. 2017;25(9):1517-1527 https://doi.org/10.3727/096504017X14859934460780
IEEE Style
J. Wang and G. Sun, “FOXO1–MALAT1–miR-26a-5p Feedback Loop Mediates Proliferation and Migration in Osteosarcoma Cells,” Oncol. Res., vol. 25, no. 9, pp. 1517-1527, 2017. https://doi.org/10.3727/096504017X14859934460780



cc Copyright © 2017 The Author(s). Published by Tech Science Press.
This work is licensed under a Creative Commons Attribution 4.0 International License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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