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Salidroside inhibits chronic myeloid leukemia cell proliferation and induces apoptosis by regulating the miR‑140‑5p/wnt5a/β‑catenin axis

  • Authors:
    • Danjun Chen
    • Cong Luo
  • View Affiliations / Copyright

    Affiliations: Department of Pharmacy, The First Affiliated Hospital of University of South China, Hengyang, Hunan 421001, P.R. China, Department of Hematology, The First Affiliated Hospital of University of South China, Hengyang, Hunan 421001, P.R. China
    Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 1249
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    Published online on: September 2, 2021
       https://doi.org/10.3892/etm.2021.10684
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Abstract

Salidroside, an active ingredient of Rhodiola rosea, exhibits antitumor effects in various types of cancer. However, the role of salidroside in chronic myeloid leukemia (CML) has not been elucidated. In the presents study, cell viability was assessed by CCK‑8 assay, while apoptosis was detected by flow cytometry. Reverse transcription‑quantitative PCR analysis was used to examine the expression levels of miR‑140‑5p in human CML cell lines. The expression levels of apoptosis and cell cycle‑associated proteins and of the wnt5a/β‑catenin signaling pathway were determined by western blot analysis. Bioinformatic analysis and luciferase reporter assays were employed to investigate the association between miR‑140‑5p and wnt5a. The results revealed that exposure of CML cells to salidroside (80 µM) inhibited cell proliferation and promoted apoptosis. In addition, salidroside treatment led to the upregulation of miR‑140‑5p expression. Furthermore, the inhibition of wnt5a/β‑catenin signaling pathway and the pro‑apoptotic effects induced by salidroside were attenuated by miR‑140‑5p silencing. Notably, wnt5a was revealed to be a direct target of miR‑140‑5p. The present findings indicated that salidroside exerted anti‑CML effects through regulating miR‑140‑5p by suppressing the wnt5a/β‑catenin signaling pathway. The present study provided evidence of the therapeutic role of salidroside in CML.
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Copy and paste a formatted citation
Spandidos Publications style
Chen D and Luo C: Salidroside inhibits chronic myeloid leukemia cell proliferation and induces apoptosis by regulating the miR‑140‑5p/wnt5a/β‑catenin axis. Exp Ther Med 22: 1249, 2021.
APA
Chen, D., & Luo, C. (2021). Salidroside inhibits chronic myeloid leukemia cell proliferation and induces apoptosis by regulating the miR‑140‑5p/wnt5a/β‑catenin axis. Experimental and Therapeutic Medicine, 22, 1249. https://doi.org/10.3892/etm.2021.10684
MLA
Chen, D., Luo, C."Salidroside inhibits chronic myeloid leukemia cell proliferation and induces apoptosis by regulating the miR‑140‑5p/wnt5a/β‑catenin axis". Experimental and Therapeutic Medicine 22.5 (2021): 1249.
Chicago
Chen, D., Luo, C."Salidroside inhibits chronic myeloid leukemia cell proliferation and induces apoptosis by regulating the miR‑140‑5p/wnt5a/β‑catenin axis". Experimental and Therapeutic Medicine 22, no. 5 (2021): 1249. https://doi.org/10.3892/etm.2021.10684
Copy and paste a formatted citation
x
Spandidos Publications style
Chen D and Luo C: Salidroside inhibits chronic myeloid leukemia cell proliferation and induces apoptosis by regulating the miR‑140‑5p/wnt5a/β‑catenin axis. Exp Ther Med 22: 1249, 2021.
APA
Chen, D., & Luo, C. (2021). Salidroside inhibits chronic myeloid leukemia cell proliferation and induces apoptosis by regulating the miR‑140‑5p/wnt5a/β‑catenin axis. Experimental and Therapeutic Medicine, 22, 1249. https://doi.org/10.3892/etm.2021.10684
MLA
Chen, D., Luo, C."Salidroside inhibits chronic myeloid leukemia cell proliferation and induces apoptosis by regulating the miR‑140‑5p/wnt5a/β‑catenin axis". Experimental and Therapeutic Medicine 22.5 (2021): 1249.
Chicago
Chen, D., Luo, C."Salidroside inhibits chronic myeloid leukemia cell proliferation and induces apoptosis by regulating the miR‑140‑5p/wnt5a/β‑catenin axis". Experimental and Therapeutic Medicine 22, no. 5 (2021): 1249. https://doi.org/10.3892/etm.2021.10684
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