Regulation of mPGES-1 composition and cell growth via the MAPK signaling pathway in jurkat cells

• Published in: Experimental and therapeutic medicine Vol. 16; no. 4; pp. 3211 - 3219
• Main Authors: Li, Yi-Qing, Chen, Jiao-Ting, Yin, Song-Mei, Nie, Da-Nian, He, Zhi-Yuan, Xie, Shuang-Feng, Wang, Xiu-Ju, Wu, Yu-Dan, Xiao, Jie, Liu, Hong-Yun, Wang, Jie-Yu, Yang, Wen-Juan, Ma, Li-Ping
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications 01.10.2018; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Analysis; Apoptosis; Cancer therapies; Care and treatment; Cell cycle; Cell growth; Development and progression; Feedback; Gene expression; Genetic aspects; Genetic regulation; Kinases; Leukemia; Proteins; Studies; T cell lymphoma; Tumors; United States > US; China; feedback; mitogen activated protein Kinase Signaling System; jurkat cell; microsomal prostaglandin-E synthase; T-cell acute lymphoblastic leukemia
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2018.6538

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.