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Article

Knockdown of p54nrb inhibits migration, invasion and TNF-α release of human acute monocytic leukemia THP1 cells

  • Authors:
    • Xiujuan Zhang
    • Changli Wu
    • Wei Xiong
    • Chunling Chen
    • Rong Li
    • Guangji Zhou
  • View Affiliations / Copyright

    Affiliations: Department of Physiology, Guangdong Medical University, Zhanjiang, Guangdong 524023, P.R. China, Department of Pathophysiology, Guangdong Medical University, Zhanjiang, Guangdong 524023, P.R. China
  • Pages: 3742-3748
    |
    Published online on: April 20, 2016
       https://doi.org/10.3892/or.2016.4756
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Abstract

54 kDa nuclear RNA- and DNA-binding protein (p54nrb) which is also called non-POU domain-containing octamer-binding protein (NONO) is known to be multifunctional involved in many nuclear processes. It was shown that p54nrb/NONO was closely related to the occurrence of erythroleukemia. Whether p54nrb/NONO plays a role in progress of human acute monocytic leukemia remains unknown. In the present study, we examined the effects of p54nrb/NONO silencing on the biological characteristics of human acute monocytic leukemia THP1 cells. The results showed that p54nrb was strongly expressed in THP1 cells, and knockdown of p54nrb slightly promoted proliferation and strongly inhibited motility and invasion of THP1 cells. Moreover, knockdown of p54nrb strongly decreased the release of TNF-α from THP1 cells by inhibiting certain process of TNF-α secretion, specially for the release of TNF-α induced by lipopolysaccharide (LPS). Notably, the infection of negative control shRNA-containing lentiviruses promoted the migration and the release of TNF-α induced by LPS in THP1 cells. All the above results demonstrated that p54nrb slightly inhibited THP1 cell proliferation, but significantly promoted migration, invasion and release of TNF-α induced by LPS in THP1 cells. The present study indicates that p54nrb is a powerful molecule involved in the regulation of cell motility and promotes the migration and invasion of THP1 cells, and it is more likely to be involved in the release of inflammatory mediators and the motility of inflammatory cells.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang X, Wu C, Xiong W, Chen C, Li R and Zhou G: Knockdown of p54nrb inhibits migration, invasion and TNF-α release of human acute monocytic leukemia THP1 cells. Oncol Rep 35: 3742-3748, 2016.
APA
Zhang, X., Wu, C., Xiong, W., Chen, C., Li, R., & Zhou, G. (2016). Knockdown of p54nrb inhibits migration, invasion and TNF-α release of human acute monocytic leukemia THP1 cells. Oncology Reports, 35, 3742-3748. https://doi.org/10.3892/or.2016.4756
MLA
Zhang, X., Wu, C., Xiong, W., Chen, C., Li, R., Zhou, G."Knockdown of p54nrb inhibits migration, invasion and TNF-α release of human acute monocytic leukemia THP1 cells". Oncology Reports 35.6 (2016): 3742-3748.
Chicago
Zhang, X., Wu, C., Xiong, W., Chen, C., Li, R., Zhou, G."Knockdown of p54nrb inhibits migration, invasion and TNF-α release of human acute monocytic leukemia THP1 cells". Oncology Reports 35, no. 6 (2016): 3742-3748. https://doi.org/10.3892/or.2016.4756
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang X, Wu C, Xiong W, Chen C, Li R and Zhou G: Knockdown of p54nrb inhibits migration, invasion and TNF-α release of human acute monocytic leukemia THP1 cells. Oncol Rep 35: 3742-3748, 2016.
APA
Zhang, X., Wu, C., Xiong, W., Chen, C., Li, R., & Zhou, G. (2016). Knockdown of p54nrb inhibits migration, invasion and TNF-α release of human acute monocytic leukemia THP1 cells. Oncology Reports, 35, 3742-3748. https://doi.org/10.3892/or.2016.4756
MLA
Zhang, X., Wu, C., Xiong, W., Chen, C., Li, R., Zhou, G."Knockdown of p54nrb inhibits migration, invasion and TNF-α release of human acute monocytic leukemia THP1 cells". Oncology Reports 35.6 (2016): 3742-3748.
Chicago
Zhang, X., Wu, C., Xiong, W., Chen, C., Li, R., Zhou, G."Knockdown of p54nrb inhibits migration, invasion and TNF-α release of human acute monocytic leukemia THP1 cells". Oncology Reports 35, no. 6 (2016): 3742-3748. https://doi.org/10.3892/or.2016.4756
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