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Isoferulic acid inhibits human leukemia cell growth through induction of G2/M‑phase arrest and inhibition of Akt/mTOR signaling

  • Authors:
    • Zhiguo Long
    • Guangjia Feng
    • Na Zhao
    • Lei Wu
    • Hongbo Zhu
  • View Affiliations / Copyright

    Affiliations: Department of Hematology, Shanghai Pudong Hospital, Fudan University, Shanghai 201399, P.R. China, Department of Pathology, Shanghai Pudong Hospital, Fudan University, Shanghai 201399, P.R. China
    Copyright: © Long et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1035-1042
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    Published online on: January 9, 2020
       https://doi.org/10.3892/mmr.2020.10926
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Abstract

Hematologic malignancy is a serious disease that develops quickly and aggressively, severely threatening human health owing to its high mortality. The current study aimed to evaluate the antitumor effects of isoferulic acid (IFA) on leukemia cells and investigate the possible molecular mechanisms. Hematologic cancer cell lines (Raji, K562 and Jurkat) were treated with IFA in a dose‑dependent manner and proliferation was measured by a cell proliferation assay. Cell cycle arrest was detected via flow cytometry using propidium iodide (PI) staining. Cell apoptosis and apoptosis‑associated signal pathways were analyzed via Annexin V/PI staining and western blot assays, respectively. IFA inhibited cell viability, induced cell apoptosis and triggered cell cycle arrest in G2/M phase in Raji, K562, and Jurkat cells in a dose‑dependent manner. In response to IFA treatment, the levels of cleaved poly(ADP‑ribose) polymerase and cleaved caspase‑3 were increased in Jurkat and K562 cells, which was associated with increased phosphorylation of Cdc2 and reduction of Cyclin B1 levels. IFA remarkably attenuated the phosphorylation of mTOR and Akt in Jurkat cells. Collectively, the present data suggested that IFA had therapeutic effects on Jurkat, K562, and Raji cells, indicating it as a promising candidate for the treatment of hematologic malignancy.
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Copy and paste a formatted citation
Spandidos Publications style
Long Z, Feng G, Zhao N, Wu L and Zhu H: Isoferulic acid inhibits human leukemia cell growth through induction of G2/M‑phase arrest and inhibition of Akt/mTOR signaling. Mol Med Rep 21: 1035-1042, 2020.
APA
Long, Z., Feng, G., Zhao, N., Wu, L., & Zhu, H. (2020). Isoferulic acid inhibits human leukemia cell growth through induction of G2/M‑phase arrest and inhibition of Akt/mTOR signaling. Molecular Medicine Reports, 21, 1035-1042. https://doi.org/10.3892/mmr.2020.10926
MLA
Long, Z., Feng, G., Zhao, N., Wu, L., Zhu, H."Isoferulic acid inhibits human leukemia cell growth through induction of G2/M‑phase arrest and inhibition of Akt/mTOR signaling". Molecular Medicine Reports 21.3 (2020): 1035-1042.
Chicago
Long, Z., Feng, G., Zhao, N., Wu, L., Zhu, H."Isoferulic acid inhibits human leukemia cell growth through induction of G2/M‑phase arrest and inhibition of Akt/mTOR signaling". Molecular Medicine Reports 21, no. 3 (2020): 1035-1042. https://doi.org/10.3892/mmr.2020.10926
Copy and paste a formatted citation
x
Spandidos Publications style
Long Z, Feng G, Zhao N, Wu L and Zhu H: Isoferulic acid inhibits human leukemia cell growth through induction of G2/M‑phase arrest and inhibition of Akt/mTOR signaling. Mol Med Rep 21: 1035-1042, 2020.
APA
Long, Z., Feng, G., Zhao, N., Wu, L., & Zhu, H. (2020). Isoferulic acid inhibits human leukemia cell growth through induction of G2/M‑phase arrest and inhibition of Akt/mTOR signaling. Molecular Medicine Reports, 21, 1035-1042. https://doi.org/10.3892/mmr.2020.10926
MLA
Long, Z., Feng, G., Zhao, N., Wu, L., Zhu, H."Isoferulic acid inhibits human leukemia cell growth through induction of G2/M‑phase arrest and inhibition of Akt/mTOR signaling". Molecular Medicine Reports 21.3 (2020): 1035-1042.
Chicago
Long, Z., Feng, G., Zhao, N., Wu, L., Zhu, H."Isoferulic acid inhibits human leukemia cell growth through induction of G2/M‑phase arrest and inhibition of Akt/mTOR signaling". Molecular Medicine Reports 21, no. 3 (2020): 1035-1042. https://doi.org/10.3892/mmr.2020.10926
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