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Chidamide induces apoptosis in DLBCL cells by suppressing the HDACs/STAT3/Bcl‑2 pathway

  • Authors:
    • Hongwei Zhang
    • Fenqing Chi
    • Keru Qin
    • Xiuli Mu
    • Lieyang Wang
    • Bin  Yang
    • Yanli Wang
    • Min Bai
    • Zhenhua Li
    • Liping Su
    • Baofeng Yu
  • View Affiliations / Copyright

    Affiliations: Department of Hematology, Cancer Hospital of Shanxi Province, Taiyuan, Shanxi 030013, P.R. China, Department of Biochemistry and Molecular Biology, Key Laboratory of Cellular Physiology of Ministry of Education, Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China
    Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 308
    |
    Published online on: February 26, 2021
       https://doi.org/10.3892/mmr.2021.11947
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Abstract

Diffuse large B‑cell lymphoma (DLBCL) is a highly heterogeneous malignant tumor type, and epigenetic modifications such as acetylation or deacetylation serve vital roles in its development. Chidamide, a novel histone deacetylase inhibitor, exerts an anticancer effect against various types of cancer. The present study aimed to evaluate the cellular effect of chidamide on a number of DLBCL cell lines and to investigate its underlying mechanism. The results demonstrated that chidamide induced the death of these cells in a concentration‑(0‑30 µmol/l) and time‑dependent (24‑72 h) manner, as determined using the Cell Counting Kit‑8 cell viability assay. Moreover, chidamide promoted cellular apoptosis, which was identified via flow cytometry and western blot analysis, with an increase in cleaved caspase‑3 expression and a decrease in Bcl‑2 expression. Chidamide treatment also decreased the expression level of STAT3 and its phosphorylation, which was accompanied by the downregulation of a class‑I histone deacetylase (HDAC) inhibitor, chidamide. Collectively, these data suggested that chidamide can be a potent therapeutic agent to treat DLBCL by inducing the apoptotic death of DLBCL cells by inhibiting the HDACs/STAT3/Bcl‑2 pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang H, Chi F, Qin K, Mu X, Wang L, Yang B, Wang Y, Bai M, Li Z, Su L, Su L, et al: Chidamide induces apoptosis in DLBCL cells by suppressing the HDACs/STAT3/Bcl‑2 pathway. Mol Med Rep 23: 308, 2021.
APA
Zhang, H., Chi, F., Qin, K., Mu, X., Wang, L., Yang, B. ... Yu, B. (2021). Chidamide induces apoptosis in DLBCL cells by suppressing the HDACs/STAT3/Bcl‑2 pathway. Molecular Medicine Reports, 23, 308. https://doi.org/10.3892/mmr.2021.11947
MLA
Zhang, H., Chi, F., Qin, K., Mu, X., Wang, L., Yang, B., Wang, Y., Bai, M., Li, Z., Su, L., Yu, B."Chidamide induces apoptosis in DLBCL cells by suppressing the HDACs/STAT3/Bcl‑2 pathway". Molecular Medicine Reports 23.5 (2021): 308.
Chicago
Zhang, H., Chi, F., Qin, K., Mu, X., Wang, L., Yang, B., Wang, Y., Bai, M., Li, Z., Su, L., Yu, B."Chidamide induces apoptosis in DLBCL cells by suppressing the HDACs/STAT3/Bcl‑2 pathway". Molecular Medicine Reports 23, no. 5 (2021): 308. https://doi.org/10.3892/mmr.2021.11947
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang H, Chi F, Qin K, Mu X, Wang L, Yang B, Wang Y, Bai M, Li Z, Su L, Su L, et al: Chidamide induces apoptosis in DLBCL cells by suppressing the HDACs/STAT3/Bcl‑2 pathway. Mol Med Rep 23: 308, 2021.
APA
Zhang, H., Chi, F., Qin, K., Mu, X., Wang, L., Yang, B. ... Yu, B. (2021). Chidamide induces apoptosis in DLBCL cells by suppressing the HDACs/STAT3/Bcl‑2 pathway. Molecular Medicine Reports, 23, 308. https://doi.org/10.3892/mmr.2021.11947
MLA
Zhang, H., Chi, F., Qin, K., Mu, X., Wang, L., Yang, B., Wang, Y., Bai, M., Li, Z., Su, L., Yu, B."Chidamide induces apoptosis in DLBCL cells by suppressing the HDACs/STAT3/Bcl‑2 pathway". Molecular Medicine Reports 23.5 (2021): 308.
Chicago
Zhang, H., Chi, F., Qin, K., Mu, X., Wang, L., Yang, B., Wang, Y., Bai, M., Li, Z., Su, L., Yu, B."Chidamide induces apoptosis in DLBCL cells by suppressing the HDACs/STAT3/Bcl‑2 pathway". Molecular Medicine Reports 23, no. 5 (2021): 308. https://doi.org/10.3892/mmr.2021.11947
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