Journal
EXPERIMENTAL AND THERAPEUTIC MEDICINE
Volume 16, Issue 4, Pages 3211-3219Publisher
SPANDIDOS PUBL LTD
DOI: 10.3892/etm.2018.6538
Keywords
feedback; jurkat cell; microsomal prostaglandin-E synthase; mitogen activated protein Kinase Signaling System; T-cell acute lymphoblastic leukemia
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Funding
- National Natural Science Foundation of China [81200342]
- Guangdong Science and Technology Department [2014A020212085, 2016A020215062]
- Natural Science Foundation of Guangdong Province [2016A030313360]
- State Scholarship Fund of China [CSC 201606380189]
- Key Laboratory of Malignant Tumor Molecular Mechanism
- Translational Medicine of Guangzhou Bureau of Science and Information Technology [163 (2013)]
- Key Laboratory of Malignant Tumor Gene Regulation and the Target Therapy of Guangdong Higher Education Institutes [KLB09001]
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Previous studies have suggested that microsomal prostaglandin E synthase-1 (mPGES-1) is highly expressed and closely associated with mitogen-activated protein kinase (MAPK) signaling pathways in various types of malignant cells. However, their expression patterns and function with respect to T-cell acute lymphoblastic leukemia (T-ALL) remain largely unknown. The present study investigated whether mPGES-1 served a crucial role in T-ALL and aimed to identify interactions between mPGES-1 and the MAPK signaling pathway in T-ALL. The results indicated that mPGES-1 overexpression in T-ALL jurkat cells was significantly decreased by RNA silencing. Decreasing mPGES-1 on a consistent basis may inhibit cell proliferation, induce apoptosis and arrest the cell cycle in T-ALL jurkat cells. Microarray and western blot analyses revealed that c-Jun N-terminal kinase served a role in the mPGES-1/prostaglandin E2/EP4/MAPK positive feedback loops. In addition, P38 and extracellular signal-regulated kinase 1/2 exhibited negative feedback effects on mPGES-1. In conclusion, the results suggested that cross-talk between mPGES-1 and the MAPK signaling pathway was very complex. Therefore, the combined regulation of mPGES-1 and the MAPK signaling pathway may be developed into a new candidate therapy for T-ALL in the future.
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