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Long non‑coding RNA TUG1 knockdown repressed the viability, migration and differentiation of osteoblasts by sponging miR‑214

  • Authors:
    • Zhitao Yao
    • Wei An
    • Adili Moming
    • Maimaitituxun Tuerdi
  • View Affiliations / Copyright

    Affiliations: Department of Oral & Maxillofacial Surgery, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang Uygur Autonomous Region 830000, P.R. China
    Copyright: © Yao et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY_NC 4.0].
  • Article Number: 203
    |
    Published online on: January 7, 2022
       https://doi.org/10.3892/etm.2022.11126
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Abstract

The maxillofacial region in the human body is susceptible to fracture and corresponding soft tissue injury. In the current study, the effect of long non‑coding RNA (lncRNA) taurine upregulated gene 1 (TUG1) on maxillofacial fracture development was investigated. In total, 50 patients diagnosed with maxillary fracture and 50 healthy volunteers were enrolled in this study. Participants' TUG1 expression level in serum was measured using reverse transcription‑quantitative (RT‑q)PCR. After transfection with small interfering (si)‑TUG1, microRNA (miR)‑214 mimic, miR‑214 inhibitor, bone morphogenetic protein 2 (BMP2) mimic or a combination, the biological behavior of osteoblasts was evaluated using MTT, Transwell assays, RT‑qPCR, flow cytometry and western blot analysis. Recovery experiments were used to explore the potential mechanism. Results demonstrated that TUG1 expression was decreased in the serum of patients with maxillary fractures. Knockdown of TUG1 repressed viability, migration and differentiation and induced apoptosis of osteoblasts. StarBase v2.0 revealed that TUG1 served as a sponge for miR‑214 and BMP2 is a direct target of miR‑214. Altogether, it was revealed that TUG1 expression was decreased in patients with maxillary fractures and TUG1 knockdown repressed the biological process of osteoblasts by sponging miR‑214.
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Copy and paste a formatted citation
Spandidos Publications style
Yao Z, An W, Moming A and Tuerdi M: Long non‑coding RNA TUG1 knockdown repressed the viability, migration and differentiation of osteoblasts by sponging miR‑214. Exp Ther Med 23: 203, 2022.
APA
Yao, Z., An, W., Moming, A., & Tuerdi, M. (2022). Long non‑coding RNA TUG1 knockdown repressed the viability, migration and differentiation of osteoblasts by sponging miR‑214. Experimental and Therapeutic Medicine, 23, 203. https://doi.org/10.3892/etm.2022.11126
MLA
Yao, Z., An, W., Moming, A., Tuerdi, M."Long non‑coding RNA TUG1 knockdown repressed the viability, migration and differentiation of osteoblasts by sponging miR‑214". Experimental and Therapeutic Medicine 23.3 (2022): 203.
Chicago
Yao, Z., An, W., Moming, A., Tuerdi, M."Long non‑coding RNA TUG1 knockdown repressed the viability, migration and differentiation of osteoblasts by sponging miR‑214". Experimental and Therapeutic Medicine 23, no. 3 (2022): 203. https://doi.org/10.3892/etm.2022.11126
Copy and paste a formatted citation
x
Spandidos Publications style
Yao Z, An W, Moming A and Tuerdi M: Long non‑coding RNA TUG1 knockdown repressed the viability, migration and differentiation of osteoblasts by sponging miR‑214. Exp Ther Med 23: 203, 2022.
APA
Yao, Z., An, W., Moming, A., & Tuerdi, M. (2022). Long non‑coding RNA TUG1 knockdown repressed the viability, migration and differentiation of osteoblasts by sponging miR‑214. Experimental and Therapeutic Medicine, 23, 203. https://doi.org/10.3892/etm.2022.11126
MLA
Yao, Z., An, W., Moming, A., Tuerdi, M."Long non‑coding RNA TUG1 knockdown repressed the viability, migration and differentiation of osteoblasts by sponging miR‑214". Experimental and Therapeutic Medicine 23.3 (2022): 203.
Chicago
Yao, Z., An, W., Moming, A., Tuerdi, M."Long non‑coding RNA TUG1 knockdown repressed the viability, migration and differentiation of osteoblasts by sponging miR‑214". Experimental and Therapeutic Medicine 23, no. 3 (2022): 203. https://doi.org/10.3892/etm.2022.11126
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