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Cimigenol depresses acute myeloid leukemia cells protected by breaking bone marrow stromal cells via CXCR4/SDF‑1α

  • Authors:
    • Bangyun Ma
    • Huibo Dai
    • Xingbin Dai
    • Shushu Qian
    • Xiaocao Sha
    • Xuemei Sun
  • View Affiliations / Copyright

    Affiliations: Department of Hematology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, P.R. China
    Copyright: © Ma et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 80
    |
    Published online on: December 30, 2022
       https://doi.org/10.3892/etm.2022.11779
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Abstract

The purpose of the present study was to evaluate cimigenol (Cim) treatment effects to cell proliferation by breaking bone marrow stromal cells (BMSCs) through C‑X‑C chemokine receptor type 4 (CXCR4)/stromal cell‑derived factor‑1α (SDF‑1α) pathway. MV‑4‑11 and U937 cell lines were used. The present study was divided into two parts. First, the cell lines were divided into normal control (NC), BMSC (cells co‑cultured with BMSCs), BMSC + DMSO, BMSC + Low (treated with 5 mg/ml Cim), BMSC + Middle (treated with 10 mg/ml Cim), BMSC + High (treated with 20 mg/ml Cim). In the second step, the cell lines were divided into NC, BMSC, BMSC + BL8040 (treated with BL8040 which inhibits CXCR4), BMSC + Cim and BMSC + Cim + BL8040. EdU positive cell numbers were measured by EdU assay and apoptosis rate by flow cytometry and TUNEL assay. Relative gene and protein expression was measured by reverse transcription‑quantitative PCR and western blotting assay. BMSCs were able to protect proliferation of cancer cells and decreased cell apoptosis compared with the NC group (P<0.001, respectively). With Cim supplement, the cell proliferation was decreased with cell apoptosis increasing compared with NC group (P<0.001 respectively). However, the anti‑tumor effects of Cim were not significantly different from the BL8040 treated groups (P<0.001, respectively). In conclusion Cim decreased acute myeloid leukemia cells protected by BMSCs through the CXCR4/SDF‑1α pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Ma B, Dai H, Dai X, Qian S, Sha X and Sun X: Cimigenol depresses acute myeloid leukemia cells protected by breaking bone marrow stromal cells via CXCR4/SDF‑1α. Exp Ther Med 25: 80, 2023.
APA
Ma, B., Dai, H., Dai, X., Qian, S., Sha, X., & Sun, X. (2023). Cimigenol depresses acute myeloid leukemia cells protected by breaking bone marrow stromal cells via CXCR4/SDF‑1α. Experimental and Therapeutic Medicine, 25, 80. https://doi.org/10.3892/etm.2022.11779
MLA
Ma, B., Dai, H., Dai, X., Qian, S., Sha, X., Sun, X."Cimigenol depresses acute myeloid leukemia cells protected by breaking bone marrow stromal cells via CXCR4/SDF‑1α". Experimental and Therapeutic Medicine 25.2 (2023): 80.
Chicago
Ma, B., Dai, H., Dai, X., Qian, S., Sha, X., Sun, X."Cimigenol depresses acute myeloid leukemia cells protected by breaking bone marrow stromal cells via CXCR4/SDF‑1α". Experimental and Therapeutic Medicine 25, no. 2 (2023): 80. https://doi.org/10.3892/etm.2022.11779
Copy and paste a formatted citation
x
Spandidos Publications style
Ma B, Dai H, Dai X, Qian S, Sha X and Sun X: Cimigenol depresses acute myeloid leukemia cells protected by breaking bone marrow stromal cells via CXCR4/SDF‑1α. Exp Ther Med 25: 80, 2023.
APA
Ma, B., Dai, H., Dai, X., Qian, S., Sha, X., & Sun, X. (2023). Cimigenol depresses acute myeloid leukemia cells protected by breaking bone marrow stromal cells via CXCR4/SDF‑1α. Experimental and Therapeutic Medicine, 25, 80. https://doi.org/10.3892/etm.2022.11779
MLA
Ma, B., Dai, H., Dai, X., Qian, S., Sha, X., Sun, X."Cimigenol depresses acute myeloid leukemia cells protected by breaking bone marrow stromal cells via CXCR4/SDF‑1α". Experimental and Therapeutic Medicine 25.2 (2023): 80.
Chicago
Ma, B., Dai, H., Dai, X., Qian, S., Sha, X., Sun, X."Cimigenol depresses acute myeloid leukemia cells protected by breaking bone marrow stromal cells via CXCR4/SDF‑1α". Experimental and Therapeutic Medicine 25, no. 2 (2023): 80. https://doi.org/10.3892/etm.2022.11779
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