Open Access

HLX affects cell cycle and proliferation in AML cells via the JAK/STAT signaling pathway

  • Authors:
    • Xia‑Yin Zhu
    • Qun‑Yi Guo
    • Min Zhu
    • Bao‑Guo Chen
    • Ling‑Yan Wang
    • Dan‑Qiong Zhang
    • Li Zhang
    • Yan‑Ping Shao
    • Wen‑Da Luo
  • View Affiliations

  • Published online on: June 9, 2020     https://doi.org/10.3892/ol.2020.11718
  • Pages: 1888-1896
  • Copyright: © Zhu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Acute myelogenous leukemia (AML) is a class of malignant tumors derived from hematopoietic stem or progenitor cells. The H2.0‑like homeobox gene (HLX) encodes transcription factors that function in promoting normal hematopoietic cell proliferation and tumor immunity. The present study analyzed the effect of downregulating the HLX on cell cycle distribution and cell proliferation in AML. Moreover, the current study detected changes in the expression of genes and proteins in the Janus kinase (JAK)/STAT signaling pathway to investigate the mechanism of the action of HLX in tumor immunity in AML. HLX expression in AML cell lines was silenced using small interfering siRNA, and MTS/PMS‑assay colorimetric assays were used to assess the effect of knockdown of HLX on AML cell proliferation. Flow cytometry was used to analyze changes in cell cycle distribution, while reverse transcription‑quantitative PCR and western blotting were used to detect changes in the expression levels of key components of the JAK/STAT signaling pathway, such as p21‑activated kinase 1 (PAK1), neuropilin 1 (NRP1), B‑cell translocation gene 1 (BTG1) and STAT5. It was found that HLX was differentially expressed in AML cell lines of various subtypes, and HLX expression was higher in the AML/M3 subtype NB4 cell line compared with the control group. Knockdown of HLX in NB4 cells significantly inhibited cell proliferation and arrested cells in the G0/G1 phase. Moreover, STAT5 protein expression, as well as NRP1 and PAK1 expression levels were downregulated, while BTG1 expression was upregulated when HLX was knocked out by siRNA. Collectively, the results suggested that downregulation of HLX may cause G0/G1 phase arrest and inhibit the proliferation of AML cells by activating the JAK/STAT signaling pathway.

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August-2020
Volume 20 Issue 2

Print ISSN: 1792-1074
Online ISSN:1792-1082

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Spandidos Publications style
Zhu XY, Guo QY, Zhu M, Chen BG, Wang LY, Zhang DQ, Zhang L, Shao YP and Luo WD: HLX affects cell cycle and proliferation in AML cells via the JAK/STAT signaling pathway. Oncol Lett 20: 1888-1896, 2020
APA
Zhu, X., Guo, Q., Zhu, M., Chen, B., Wang, L., Zhang, D. ... Luo, W. (2020). HLX affects cell cycle and proliferation in AML cells via the JAK/STAT signaling pathway. Oncology Letters, 20, 1888-1896. https://doi.org/10.3892/ol.2020.11718
MLA
Zhu, X., Guo, Q., Zhu, M., Chen, B., Wang, L., Zhang, D., Zhang, L., Shao, Y., Luo, W."HLX affects cell cycle and proliferation in AML cells via the JAK/STAT signaling pathway". Oncology Letters 20.2 (2020): 1888-1896.
Chicago
Zhu, X., Guo, Q., Zhu, M., Chen, B., Wang, L., Zhang, D., Zhang, L., Shao, Y., Luo, W."HLX affects cell cycle and proliferation in AML cells via the JAK/STAT signaling pathway". Oncology Letters 20, no. 2 (2020): 1888-1896. https://doi.org/10.3892/ol.2020.11718